The idea of creating new forms of life has been both an exhilarating and terrifying idea in storytelling for ages. Think of the monster that Frankenstein created in Mary Shelleys book from 1818. Or, to consider a more recent example, the robotic androids that seem to gain sentience in the videogame Detroit: Become Human. While such examples are currently science fiction and are not exactly up to our rigorous scientific standards, some researchers believe that developments in biomedical research may eventually confront us with similar forms of “life” or “sentience”, namely in the form of organoids. While these biotechnical constructs are only somewhat like the living things that we now know, increasing similarities might soon make us consider the duck test: “If it looks like a duck, swims like a duck, and quacks like a duck” …should we ever deem it a duck? And at what point do we then have responsibilities towards that duck?
Organoids
Organoids are small, three-dimensional tissue cultures, composed of organ-specific cell types. As their name suggests they are organ-like but do not look like little versions of organs. Organoids are a few millimeters wide “blobs”;[i] clusters of cells that self-organize in ways that resemble aspects of real organs. By guiding stem cells to differentiate into specific tissues, scientists have created kidney, lung, ocular, tongue, and many other types of organoids.
These models are already used to study the development of organs and disease development. They also show promise for drug testing and personalized medicine. Some scientists claim that organoids might become even better models than animal models, especially when these organoids are based on material from potential patients. At some point, they might more accurately predict which treatments will work for a specific person.[ii] However, realizing this promise requires organoids to become increasingly complex over time.
Increasing complexity
One example of increasing complexity that especially sparks the imagination is the human brain organoid (HBO). The development of neural structures incurs the vision that, potentially, some form of sentience could develop in the future.[iii]
Another increase of complexity is seen in the development of combined organoids. Once we bring organoids together, in the case of assembloids or multiple-organoids-on-a-chip, some form of interaction between the models starts to occur.[iv] This could be useful to model the digestive tract, for example, or could also be done by involving HBOs with other models. A blob of cells connected to another blob of cells might not sound much like “creating life” or “a sentient being”. However, once organoids start to become even more complex, how we feel about them could start to become more muddled.
We may start asking whether highly complex organoids are merely scientific tools, or whether they become entities to which we owe some form of responsibility. At what point does something stop being a “thing” and should it be seen as a living thing?
These intuitions touch the concept of moral status. An entity can be considered to have a moral status, if it matters from a moral point of view[v]. This tells us how something ought to be treated. If you feel it is wrong to kick a dog, while not feeling bad for kicking a rock, this is determined by the first having a certain moral status that the latter does not. You have a moral responsibility to treat entities with a higher moral status differently.
For example, we could wonder if models that involve neural organoids in some capacity might, at one point, experience pain or suffering during experiments. That could make us culpable for any harm incurred or responsible for its wellbeing. Still, how would we even know about their experience? The HBOs cannot express their pain and we are unsure whether their patterns of activity are comparable to our brains. As HBOs could become increasingly sophisticated, H.T. Greely asks in parallel to the duck test: “[i]f it looks like a human brain and acts like a human brain, at what point do we have to treat it like a human brain – or a human being?”[vi]
However, many scientists that use organoids, including those working with HBOs, state that these concerns are overblown.[vii] Neural organoids are in no way as complex as brains; they only represent very specific parts of a brain and even then, only consist of a small cluster of cells. Still, while it is a fraction of human brains, some already have the same or larger number of cells compared to brains of honeybees.[viii]
When do duck-likes become ducks?
Back to our duck test: if the things we are dealing with are quite duck-like and might become more like ducks, are we not possibly dealing with future ducks? We simply do not know yet. The worries we mentioned might never come to align with reality, or it could somehow already be happening without us realizing right now.
So, while it is prudent to explore potential futures, we need to assess whether this is realistic. Just because something seems like another, does not mean it actually is fundamentally similar. The philosopher Tomasz Żuradzki warns those pleading for strict precautionary measures to not only focus on under-caution, but also over-caution.[ix] Are we creating a panic that is based solely on speculation? If this science-fiction never becomes reality, we might be hindering important progress with our precautions and fears of inflicting harm.
Preparing properly
This discussion might seem highly hypothetical, but has an important preparatory function. It helps to think ahead of scientific innovation, but also not give into duck-anxieties without proper reflection. This includes responsible communication on organoids, without giving into scientific hype or sensationalized concern.[x] So yes, we need to warn each other not to create an incomprehensible new monster of Frankenstein. At the same time, we need to work together to make sure we do not hinder important progress in health innovation.
[i] Clevers, H. (2016). Modeling development and disease with organoids. Cell, 165(7), 1586-1597.
[ii] Perkhofer, L., Frappart, P. O., Müller, M., & Kleger, A. (2018). Importance of organoids for personalized medicine. Personalized Medicine, 15(6), 461-465.
[iii] Ohayon, E. L., Tsang, P. W., & Lam, A. (2019). A computational window into the problem with organoids: approaching minimal substrates for consciousness. Neuroscience, 2019.
[iv] Pașca, S. P., Arlotta, P., Campbell, P., Charo, A., Evans, J. H., Farahany, N., Gage, F.H., Dofrey-Smith, P., Hyun, I., Kriegstein, A., Melloni, L., Ming, G., Moreno, J.D., Sugarman, J., Temple, S., Testa, G. & Greely, H. T. (2025). The need for a global effort to attend to human neural organoid and assembloid research. Science, 390(6773), 574-577. DOI: 10.1126/science.aeb1510
[v] Jaworska, A. and J. Tannenbaum. (2023)."The Grounds of Moral Status", The Stanford Encyclopedia of Philosophy (Spring 2023 Edition), Edward N. Zalta & Uri Nodelman (eds.). https://plato.stanford.edu/archives/spr2023/entries/grounds-moral-status/.
[vi] Greely, H. T. (2021). Human brain surrogates research: the onrushing ethical dilemma. The American Journal of Bioethics, 21(1), 34-45:34.
[vii] Belblidia, N. (2026). As Brain Organoid Science Grows More Complex, So Do the Questions. Undark Magazine. Last accessed 3-3-2026 via: https://undark.org/2026/02/26/brain-organoids-big-questions/
[viii] Pașca, S. P., Arlotta, P., Campbell, P., Charo, A., Evans, J. H., Farahany, N., Gage, F.H., Dofrey-Smith, P., Hyun, I., Kriegstein, A., Melloni, L., Ming, G., Moreno, J.D., Sugarman, J., Temple, S., Testa, G. & Greely, H. T. (2025). The need for a global effort to attend to human neural organoid and assembloid research. Science, 390(6773), 574-577. DOI: 10.1126/science.aeb1510
[ix] Żuradzki, T. (2021). Against the precautionary approach to moral status: the case of surrogates for living human brains. The American Journal of Bioethics, 21(1), 53-56.
[x] Bassil, K. (2024). The end of ‘mini-brains’! Responsible communication of brain organoid research. Molecular Psychology: Brain, Behavior, and Society, 2(13), 13-16.
Movement is fundamental to life. Every step we take, every stretch, and every shift in posture generates mechanical forces that cells constantly sense and respond to. In musculoskeletal tissues, these forces are not merely passive background signals - they actively regulate metabolism, extracellular matrix (ECM) production, and overall tissue homeostasis.
My PhD project explores how we can recreate these mechanical cues using dynamic biomaterials. Specifically, I develop hydrogels that can reversibly swell and shrink, mimicking the cyclic biomechanical changes naturally experienced by tissues in the body. Rather than acting as static scaffolds, these materials create an active and changing microenvironment for cells.
As the hydrogels swell and contract, they alter hydrostatic pressure, nutrient transport, and waste removal, exposing cells to controlled mechanical stimulation. This provides a powerful platform to study mechanosensing, the process by which cells sense physical forces and convert them into biochemical signals that influence intracellular signaling pathways, gene expression, and cellular behavior, including proliferation, migration, differentiation, and extracellular matrix remodeling. Together, these responses are critical for regulating tissue development, maintaining homeostasis, and driving regenerative processes following injury.
This is especially relevant for cartilaginous tissues such as cartilage and the nucleus pulposus of the intervertebral disc. These tissues are avascular, meaning they lack direct blood supply and rely entirely on diffusion for nutrient delivery and waste removal. As a result, they have low metabolic activity and very limited regenerative capacity, making degeneration difficult to reverse.
My project supports the DRIVE-RM mission by providing a controllable in vitro platform to study how mechanical cues influence regeneration in load-bearing tissues under pathological conditions, such as cartilage and intervertebral disc degeneration. By engineering hydrogels that mimic dynamic tissue loading, this work helps uncover how biomechanical signals regulate cellular behavior, extracellular vesicle function, and tissue homeostasis. These insights can guide the development of regenerative biomaterials and localized therapies for tissues with limited intrinsic healing capacity.
This research is inherently interdisciplinary. Developing and characterizing these dynamic systems requires expertise in supramolecular chemistry, material science, cell biology, mechanobiology, and extracellular vesicle research, since extracellular vesicles are increasingly recognized as important mediators of tissue repair, regeneration, and cell-to-cell signaling. Collaborations within the consortium enable the integration of advanced hydrogel design with biological validation and translational perspectives.
What excites me most is the idea that materials can do more than support cells structurally - they can actively instruct them. Understanding how physical forces shape regenerative signaling opens exciting opportunities to engineer materials that harness the body’s own repair mechanisms.
By combining dynamic biomaterials with mechanobiology, this project aims to unlock how mechanical stimulation can drive regenerative signaling in tissues with limited healing potential.
Articular cartilage (AC) plays a crucial role in enabling smooth and pain‑free body movement through efficient and frictionless load transfer in our joints. However, due to the lack of blood vessels and low initial cell numbers, cartilage tissue has almost no capacity to heal itself once damaged. Even small injuries can progress to larger defects over time, ultimately contributing to degenerative joint diseases such as osteoarthritis (OA). With OA affecting hundreds of millions of people worldwide, the need for effective AC regeneration strategies is greater than ever.
Current clinical treatments for cartilage defects (e.g. autologous chondrocyte implantation) often result in fibrocartilage and a disorganized, isotropic tissue structure that cannot endure the same mechanical loads as native hyaline cartilage, leading to failure over time. Consequently, previous research has highlighted the importance for guiding the characteristic zonal collagen fiber alignment within engineered or regenerated cartilage to enhance its mechanical durability and strength. This leads to the following key question:
Is it possible to guide cartilage growth via physical biomaterials-based cues to achieve the characteristic zonal collagen alignment? Embedded in research domain 2 and part of the in-situ musculoskeletal regeneration subtopic within DRIVE-RM, this is one of the main research questions I will focus on.
My project will revolve around guiding structural organization and remodeling of engineered neocartilage by using a modular, bottom-up tissue engineering approach. This technique combines tunable microgels with cartilage microtissues.
In the context of AC tissue engineering, cartilage organoids have emerged as powerful building blocks for creating larger tissue constructs. These small, highly controlled 3D cellular aggregates mimic key features of native cartilage, including cell–cell interactions and matrix deposition. By mixing hydrogel microparticles (i.e. microgels) with defined shapes and thermoresponsive properties to the microtissues, we aim to better control the organoid growth, fusion and overall tissue organization.
Within DRIVE-RM, we collaborate closely with Prof. Dr. Tina Vermonden and Sanne van de Looij (Utrecht University). This collaboration supports valuable knowledge exchange about advanced hydrogels in the context of cartilage tissue engineering, which is a fundamental part of my project.
I am excited to be part of this research journey in the field of regenerative medicine. I believe that my project will help to further understand how cartilage tissue architecture develops and how it can be controlled. Ultimately, this may support the development of future injectable and tunable regenerative therapies for cartilage repair.
What if we could harness the body’s own immune system to repair damaged blood vessels? This idea lies at the heart of my research. Namely, helping the body rebuild its own vessels using smart materials and the power of the immune system. Every year millions of people worldwide are affected by cardiovascular diseases. For many patients, this means surgery to replace blocked or damaged blood vessels. However, current replacements, especially for small diameter vessels, come with a variety of potential complications such as infections, inflammation and failure over time. To address this issue, my research focuses on a new and promising approach.
To better understand this process, scientists have traditionally focused on how “first-responder” immune cells such as macrophages react to these smart implants, I am investigating the role of T lymphocytes, or simply T cells. These cells act like the “generals” of the immune system. Given their important role, one of my goals is to understand how they communicate with other cells to drive the process of blood vessel regeneration. By deciphering this conversation and identifying key processes, we can design materials that will guide the body to heal itself.
This research project is part of a larger effort within the DRIVE-RM consortium to develop regenerative therapies by understanding how the body heals under challenging conditions. By learning how to control immune responses through material design, we are moving from simply “patching” a patient to creating implants that actively promote healing. More specifically, I am looking for ways to flip the “switch” from inflammation to tissue regeneration. This knowledge is crucial for creating a new generation of “off-the-shelf” cardiovascular implants.
Given the scope of this project, this puzzle is too big for one lab, so collaboration is essential. I work closely with experts in material sciences at the TUe who design and produce the biomaterials, as well as clinicians and biologists who help translate our findings into real-world applications. These partnerships provide opportunities to test ideas that would not be possible withing a single field.
Probably the most exciting part of this project is the idea that we can “talk” to the immune system using these materials. Instead of suppressing or fighting immune system, we can instead guide it to become a powerful tool for healing. This reflects a major shift in how we think about medicine. It’s not about just fixing what’s broken but enabling the body to rebuild itself.
My research unlocks (or ‘aims to) the secret language between T-cells and materials, enabling us to transform synthetic implants into living, self-healing blood vessels that can last a lifetime
Imagine jumping up and down 3 billion times in a row. Sounds impossible, right?
And yet, that is exactly what our heart does during the course of a life! From our first heartbeat until we reach the end of our lifespan, our heart contracts and relaxes non-stop. Unfortunately, the heart has a major limitation. Unlike other tissues in your body, the human adult heart lacks the ability to replace damaged tissue with new fully functional muscle. Instead, after injury such as a myocardial infarction, the damaged area dies and the tissue is replaced by a rigid scar. While this may confer some initial protection by maintaining the structural integrity of the heart, the newly formed scar cannot contract and imposes mechanical restraints that reduces heart function and places an additional burden on the remaining heart tissue. Over time, this reduction in function can lead to heart failure, which is the leading cause of death worldwide.
But is this limitation universal? While common lab mouse (Mus musculus) and humans share this same problem, our lab discovered that another rodent species, the spiny mouse (Acomys cahirinus), has evolved a way to adapt to this situation. After a myocardial infarction, spiny mice also form an initial scar, but the damage remains limited and the heart gradually recovers its function over time.
Why does one heart struggle while another adapts? Our aim is to uncover this question. We are trying to understand what molecular features allow some hearts to cope better with injury and whether these principles can eventually help human hearts recover more successfully.
In this regard, a key focus of our work is the dialogue between cardiomyocytes (the contractile cells of the heart) and their surrounding environment. Since cells do not act alone, their behaviour is shaped by the signals and conditions around them. We investigate how these interactions can influence cardiac dysfunction or repair. To explore these cell–environment interactions in greater depth, we have established a collaboration with Prof. Jos Malda and Prof. Carlijn Bouten, whose expertise in biomaterials and tissue engineering enables us to better understand the influence of the cardiac microenvironment.
What excites me about our research is the fact that new discoveries provide knowledge that could have a great impact for patients. For many years, studies have tried to restore the damaged area of the heart so it becomes indistinguishable with a healthy one. Our model teaches us that scarring does not always correlate with maladaptive repair, and that the mechanical and biochemical properties of a scar can also stimulate cellular repair and support contractile function. In other words, a heart does not need to look exactly as it did before the injury to function well. If we understand how the spiny mouse maintains a better cardiac function after injury, we might be able to recapitulate this more forgiving environment in human hearts suffering from ischemic heart disease.
In the last two decades, three-dimensional (3D) cell culture has become a central laboratory method. Across laboratories and institutes, researchers use 3D cell culture to answer questions about how tissues form, function, and repair themselves.
While many tissue engineering strategies have struggled to generate complex tissue models, a more effective approach builds on the natural ability of stem cells to self-organize. With the right, well-defined signals, stem cells can form multicellular patterns, compartments, and functional circuits that more closely resemble what they do in the body. The rise of organoids reflects this conceptual and practical shift. Organoids are miniature, simplified organ-like tissues grown from stem cells in the lab that mimic key features of real organs. They can contain highly functional cell types and broaden the range of cell types that can be generated and maintained in the lab, including types that were previously hard to obtain. Yet organoids often develop variable, hard-to-predict structures at larger scales. Contributing factors include poorly defined matrices and culture conditions, which still lack the local and time-sensitive control seen in embryonic development.
A new generation of lab-grown models could help close these gaps by following developmental paths more closely. Stem cell-derived embryo models show that shape and function can arise together in a tightly linked way, reflecting key morphological changes during early development. So far, these models mainly capture only the earliest developmental stages, but the Morphogenetic Micro Engineering team at the MERLN Institute aims to extend them to learn more about organogenesis, the formation of organs. If bioengineered tissues can be guided through key developmental milestones in the lab, it may be possible to generate physiologically relevant tissue analogues with structures that more accurately reflect early organ development.
Reaching this goal would open major opportunities. It would enable functional and anatomically accurate multicellular models for studying human development, organ formation, and regeneration. The role of environmental factors in causing congenital malformations could be investigated systematically, and tissues that are both functionally mature and anatomically correct could eventually be engineered for transplantation.
To get there, cell culture systems must improve substantially. We need new tools that guide stem cells with precise control over space and time, similar to the complex and fast-changing environment of developing tissues in a living organism. Our work focuses on developing such innovative cell culture tools that allow advanced 3D cell culture models to move through key morphological events step by step. Together, these capabilities create conditions where in vitro morphogenesis becomes something we can reliably design for. This will be a key step in connecting stem cell-derived embryo models with regenerative medicine.
Achieving this goal requires a multidisciplinary effort spanning stem cell biology, developmental biology, bioengineering, physics, computation, and clinical science. DRIVE-RM is a consortium built for this moment. Its cross-disciplinary structure and shared infrastructure support progress on problems that single laboratories cannot solve alone.
The age of 3D cell culture has shown what becomes possible when we work with biological complexity rather than avoiding it. The coming age of in vitro morphogenesis will be defined by systems that reproduce the coordinated “dance” of development and deliver the right signals in a changing spatial and temporal context to generate functional tissues with complex structures.
By simulating biological processes, computational models help researchers understand and predict how cells make decisions, how they work together in processes such as tissue development and adaptation, and how tissue organization affects function [1]. They can even estimate quantities that are difficult or impossible to measure experimentally, such as mechanical stresses within tissues, and thereby uncover how these factors drive regeneration.
In this way, computational models make in vitro and in vivo experiments more effective. They help design more efficient studies, reduce trial and error, and bridge multiple biological scales — from molecules and cells to tissues, organs, and entire systems to enable advanced analysis of experimental outcomes. There are many types of computational approaches, but they can be broadly divided into two categories: black box and white box models. Black box approaches, such as those based on artificial intelligence (AI), use data-driven methods to identify patterns and make predictions. White box approaches are based on fundamental principles — like physics and biology — to describe mechanisms and processes directly.
The research groups of both Aurélie Carlier (MERLN, Maastricht University) and Sandra Loerakker (TU/e) are mainly working on white box models. Within DRIVE-RM, Sandra and Aurélie are exploring collaborations where a PhD student will work in each institute and the projects are aligned to strengthen each other.
Within Aurélie’s research group at Maastricht University, the focus lies on ordinary and partial differential equation models and stochastic agent-based models. These are used to study how cells interact with each other and with their environment across different scales. At the subcellular level, the group has demonstrated how the size, distribution, and lifetime of cell adhesions influence YAP phosphorylation — a key regulator of cell behavior [2]. At the cellular level, they have shown that both the overall density and the local clustering of integrin ligands play a role in stem cell regulation [3]. At the tissue level, their work revealed how feedback mechanisms can help control the foreign body reaction and limit fibrosis [4]. To further refine their predictions, the group is now investigating the role of mechanical forces in these processes and is exploring collaborations with Sandra’s group to integrate experimental and computational insights.
Sandra’s research group at Eindhoven University of Technology develops mechanistic (white box) models to understand and predict how tissues grow and remodel in response to mechanical factors, and leverage these insights to improve regenerative strategies. The group particularly focuses on linking detailed mechanobiological processes at the subcellular level to tissue-scale growth and remodeling, with cardiovascular regenerative medicine as main application area. Using insights obtained from computational models, the group has identified a superior design for tissue-engineered heart valves, for which in vivo studies indeed demonstrated radically improved valve remodeling and functionality [5]. The group also pioneered the development of experimentally-informed computational models to analyze how cell-cell communication via Notch regulates cardiovascular tissue adaptation [6,7]. The group is currently developing computational methods to analyze and predict the transformation of biomaterials into living tissues, by integrating insights into mechanobiological processes into mechanistic models of mechano-regulated regeneration. The expertise of Aurélie’s group on modeling detailed intracellular processes may offer exciting opportunities for collaboration via DRIVE-RM.
The above examples illustrate the wide variety of computational techniques, and their huge potential to advance the regenerative medicine field, especially when integrated with experimental research. In the future, we envision that the AI-driven and white box techniques will be integrated into hybrid approaches, harnessing the best of both worlds to bring regenerative medicine to the next level and realize the full potential of digital twins to enable successful and predictable regeneration.
[1] Post, J.N., Loerakker, S., Merks, R.M.H., Carlier, A. (2022) Implementing computational modeling in tissue engineering: where disciplines meet. Tissue Engineering Part A, https://doi.org/10.1089/ten.TEA.2021.0215
[2] Jafarinia, H., Shi, L., Wolfenson, H., Carlier, A. (2024) YAP phosphorylation within integrin adhesions: insights from a computational model. Biophysical Journal, DOI: 10.1016/j.bpj.2024.09.002
[3] Zhang, X., Karagöz, Z., Swapnasrita, S., Habibovic, P., Carlier, A., van Rijt, S. (2023) Development of mesoporous silica nanoparticle-based films with tunable arginine-glycine-aspartate peptide global density and clustering levels to study stem cell adhesion and differentiation. ACS Appl Mater Interfaces, https://pubmed.ncbi.nlm.nih.gov/37527490/
[4] Marradi, M., van Griensven, M., Beijer, N., de Boer, J., Carlier, A. (2025) Towards predicting implant-induced fibrosis: A standardized network model of macrophage-fibroblast interactions. Computational and Structural Biotechnology Journal, https://doi.org/10.1016/j.csbj.2025.07.022
[5] Emmert M.Y., Schmitt B.A., Loerakker S., Sanders B., Spriestersbach H., Fioretta E.S., Bruder L., Brakmann K., Motta S.E., Lintas V., Dijkman P.E., Frese L., Berger F., Baaijens F.P.T., Hoerstrup S.P. (2018) Computational modeling guides tissue-engineered heart valve design for long-term in vivo performance in a translational sheep model. Science Translational Medicine, https://doi.org/10.1126/scitranslmed.aan4587
[6] Loerakker S, Stassen O.M.J.A., Ter Huurne F.M., Boareto M., Bouten C.V.C., Sahlgren C.M. (2018) Mechanosensitivity of Jagged-Notch signaling can induce a switch-type behavior in vascular homeostasis. PNAS, https://doi.org/10.1073/pnas.1715277115
[7] Van Asten J.G.M., Latorre M., Karakaya C., Baaijens F.P.T., Sahlgren C.M., Ristori T., Humphrey J.D., Loerakker S (2023) A multiscale computational model or arterial growth and remodeling including Notch signaling. Biomechanics and Modeling in Mechanobiology, https://doi.org/10.1007/s10237-023-01697-3
At Eindhoven University of Technology, my research uses 3D cardiac models to study how mechanical forces influence the organization of the extracellular matrix and cells. Through our interdisciplinary approach in mechanobiology, tissue engineering and biofabrication, I hope to uncover strategies to guide the restoration of healthy cardiac anisotropy, promote tissue repair, and prevent maladaptive remodeling.
Beyond research, I am deeply committed to connecting science with society. Since my PhD, I’ve co-led an initiative that brings together early-career Spanish researchers at the University of Cambridge each year: the ‘From Science to Society workshop (FS2S)’. Last month, we celebrated its fifth edition, hosted at Downing College of Cambridge University and supported by the Rafael del Pino Foundation.
The workshop was born from a simple but pressing idea. As a Spanish scientist who has studied and worked both at home and abroad, I’ve seen first-hand the difference that international exposure and mentorship can make. Together with a colleague from my undergraduate studies, we founded FS2S to help young scientists in Spain access those opportunities — promoting innovation, science policy, and academia–industry collaboration as essential drivers of scientific progress.
Achieving this vision required perseverance and teamwork. We sought funding to make the event financially accessible, believing that talent should never depend on means. But seeing the impact on participants — many of whom later joined international labs or created their own startups from scratch — has been the most rewarding outcome. Today, FS2S welcomes about 30 participants each year and has grown into a national platform for scientific dialogue and leadership.
Each edition features inspiring speakers from academia, biotech, and science policy. This year’s program included Kai Stoeber from Johnson & Johnson Innovation, who discussed innovation in disease prevention; Cheryl Smythe from Altos Labs, sharing how to build inclusive and creative research environments; and Florian Markowetz, Professor of Computational Oncology at the University of Cambridge, exploring how academic knowledge can improve patient care through partnerships with industry. Additional talks explored patent protection (Camille Terfve), bridging science and entrepreneurship (Agata Nyga), and the power of international collaboration and science diplomacy (José María Robles Fraga and Anna Fumarola).
What began as a small initiative between two friends has evolved into a vibrant platform connecting Spanish researchers across disciplines and borders. FS2S continues to grow as a space for learning, exchange, and inspiration — a testament to what young scientists can achieve when given the chance.
Through my research at DRIVE-RM and my outreach work with FS2S, I hope to contribute both to understanding how the heart heals and to strengthening the scientific community that makes this progress possible. Whether engineering heart tissues in the lab or creating opportunities for others to grow, my goal remains the same: to help science reach further — into new discoveries, and into society itself.
Want to learn more about this initiative? https://www.youtube.com/watch?v=0WDXSeQ-VjQ
How can we print an organ? That is the central question guiding my research as a new PhD candidate for DRIVE-RM. In particular, my interest lies in the fabrication of a kidney, the organ responsible for filtering blood and producing urine. With its million tiny filters and tubes, this organ has an intricate structure that so far has not been replicated to its full extent.
The first step towards printing a kidney lies in regenerating kidney tissue. In the RMU nephrology group, we already know how to regrow miniature pieces of kidney tissue derived from a patient’s own urine. Since they mostly represent properties of a kidney tubule, we call them tubule organoids, or in short: tubuloids. I will research how blood vessels can be connected to these tubuloids. If the ultimate goal is to use tubuloids in living patients, blood vessel formation is an important step - it will provide the tubuloids with oxygen and nutrients. One approach is to learn from other animals. For instance, I will try if a blood-rich membrane from chicken eggs can vascularise tubuloids and take lessons from that.
As a next step, biofabrication technologies might help us mimic the kidney’s architecture more closely. The hypothesis is that placing cells in a biomimetic microstructure will influence how much they regain their kidney function. For instance, we could try to suspend tubuloids in printable ink (extrusion-based bioprinting), or evaluate how they behave on a preprinted scaffold (melt electrowriting). These techniques have been utilised extensively by the Malda-group, albeit mostly for musculoskeletal tissue. My mission is to bring these techniques towards the kidney realm, trying to find crossover topics between Prof Malda’s work in biofabrication and Prof Verhaar’s work in kidney regeneration.
Seeing that multidisciplinarity is a key part of my project, I would like to take this opportunity to highlight my drive to establish interinstitutional collaboration. Mathematical modelling, clinical translation, ethics or even policy making, I would be happy to connect with any adjacent field to kidney biofab.
As a medical doctor, I have seen many patients suffering from chronic kidney disease. Some of them were dependent on tri-weekly dialysis treatment, others on immunosuppressants after transplants. All of them experienced a considerable impact on their quality of life. For the future, I hope that it will be possible to offer a personalised, lab-grown kidney to all those in need of one.
What thrills me most about regenerative medicine is how research lines can intersect. It demands speaking each other’s language, sharing knowledge and supporting each other as a community. Not only my project has been designed as a combination of biology, engineering and medicine; the entire consortium is based on interdisciplinarity. Ultimately, this collaborative approach is what will once bring a bioprinted kidney from bench to bedside.
Regenerative medicine is about understanding how cells, tissues and organs are formed and using that knowledge to rebuild tissues and help patients that have lost them through injury or disease. To do that, we can be inspired by nature’s experts in regeneration.
In the lakes of Mexico City lurks an animal that is naturally capable of things we can only dream of as humans. The axolotl (a type of salamander) can regenerate almost all of its body parts, including arms, legs, jaw, spinal cord and brain. What makes axolotls even more fascinating is that, biologically speaking, they aren’t that different from humans. We share many genes and cell types, like in the limbs and internal organs. In the Otsuki lab at the Hubrecht Institute, Utrecht, we aim to better understand how axolotls regenerate.
Specifically, we study how axolotls regenerate their jaws and limbs. These are both skeleton-containing body parts with similar cell type composition, which makes them interesting to compare in regenerative studies. We study the cell types that are needed for regeneration, and the genes and molecules involved in this process. While limb and nervous system regeneration has been studied extensively in the last 100 years, jaw regeneration is still relatively uncharted, even among axolotl researchers.
By comparing our new findings in jaw regeneration to the process of limb regeneration, we hope to understand how these processes compare. If they prove similar between jaw and limb, maybe we will come closer to understanding some universal processes for body part regeneration. If jaw and limb regeneration prove to be vastly different processes, it will be interesting to see why such differences occur, and how we can learn from them to regenerate different human tissue types.
Looking at nature provides a springboard for future innovations in therapies for patients. Working with DRIVE-RM makes it possible for us to communicate and collaborate with scientists who can use their ethical, technological and/or clinical expertise to translate our findings into effective therapies. Major breakthroughs in science require a multidisciplinary approach, which means combining our strengths to ensure a better future for patients. I hope that together, we can catalyze this knowledge into safe and reliable regenerative therapies that will change the future.
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