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.
