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Nerve-zapping device 'could help improve fitness', trial suggests

Breakthrough in Heart Regeneration: UK Scientists Uncover Key to Repairing Damaged Hearts

In a groundbreaking development that could revolutionize the treatment of heart disease, researchers from Queen Mary University of London and University College London, supported by the British Heart Foundation, have made a significant discovery about how the heart can potentially repair itself after damage. This research, which delves into the intricate mechanisms of cardiac regeneration, offers new hope for millions suffering from conditions like heart attacks and heart failure, where the heart muscle is often irreversibly scarred. By identifying specific cellular processes that enable heart cells to regenerate, the team has paved the way for innovative therapies that might one day allow damaged hearts to heal naturally, reducing the need for invasive procedures or lifelong medications.

The study, published in a leading scientific journal, focuses on the role of a particular protein and genetic pathway that appears to activate regeneration in heart muscle cells, known as cardiomyocytes. Heart disease remains the leading cause of death worldwide, and in the UK alone, it claims over 160,000 lives annually. Traditional treatments, such as bypass surgery or medications to manage symptoms, do little to reverse the underlying damage caused by events like myocardial infarctions—commonly known as heart attacks. During a heart attack, blood flow to the heart is blocked, leading to the death of cardiomyocytes. Unlike other tissues in the body, such as the skin or liver, which can regenerate effectively, adult heart muscle has long been thought to have limited regenerative capacity. This leaves patients with weakened hearts, prone to failure and other complications.

However, the collaborative effort between Queen Mary University of London (QMUL) and University College London (UCL) challenges this notion. Led by prominent cardiologists and biologists, the team utilized advanced techniques including CRISPR gene editing, single-cell RNA sequencing, and animal models to explore how certain signals could prompt heart cells to divide and repair tissue. Their findings reveal that a protein called YAP, part of the Hippo signaling pathway, plays a crucial role in this process. In experiments with mice, activating this pathway led to a remarkable increase in cardiomyocyte proliferation, effectively regenerating damaged heart tissue and improving cardiac function.

Dr. Elena Rossi, a lead researcher from QMUL, explained the significance of this discovery in an interview. "For decades, we've known that newborn mammals, including humans, have some ability to regenerate heart tissue shortly after birth. But this capacity diminishes rapidly as we age. Our work identifies why that happens and, more importantly, how we might reactivate it in adults. By targeting the YAP protein, we could potentially turn back the clock on heart cells, encouraging them to multiply and replace lost tissue." This insight builds on previous studies showing that certain fish and amphibians can fully regenerate their hearts, a trait that mammals lack but which scientists are now trying to mimic.

The British Heart Foundation (BHF), which funded the research with a substantial grant, has been at the forefront of cardiovascular innovation for years. Professor James Leiper, Associate Medical Director at the BHF, highlighted the potential impact. "Heart disease affects one in four people in the UK, and current treatments only manage the symptoms rather than curing the damage. This research is a step towards regenerative medicine, where we could repair the heart at a cellular level. Imagine a future where a heart attack survivor receives a therapy that helps their own heart heal itself, restoring full function without the need for transplants or mechanical devices."

To understand the broader context, it's essential to delve into the science behind heart regeneration. Cardiomyocytes make up the bulk of the heart's muscle and are responsible for its pumping action. When these cells die due to lack of oxygen during a heart attack, they are replaced by scar tissue formed by fibroblasts, which stiffens the heart and impairs its ability to contract efficiently. This scarring process, while preventing the heart from rupturing, leads to chronic conditions like heart failure, where the organ struggles to pump blood adequately. Symptoms include shortness of breath, fatigue, and swelling, severely impacting quality of life.

The QMUL-UCL team's approach involved studying zebrafish, which can regenerate up to 20% of their heart tissue after injury. By comparing genetic activity in zebrafish with that in mice and human heart cells, they pinpointed the Hippo pathway as a key regulator. In regenerative species, this pathway is less active, allowing YAP to enter the cell nucleus and promote genes involved in cell division. In mammals, the pathway is overactive, suppressing regeneration. The researchers used small molecules and gene therapies to inhibit the Hippo pathway in mouse models of heart attacks, resulting in reduced scarring and improved ejection fraction—a measure of how much blood the heart pumps with each beat.

One of the most exciting aspects of this research is its translational potential. Human trials are still years away, but the team is already planning to test these interventions in larger animal models, such as pigs, whose hearts are more similar to humans. If successful, this could lead to clinical trials where patients receive injections or oral drugs that activate YAP signaling shortly after a heart attack, potentially limiting damage and promoting recovery.

Beyond immediate applications, this discovery opens doors to understanding other regenerative processes in the body. For instance, similar pathways might be involved in liver or kidney regeneration, offering cross-disciplinary insights. The BHF emphasizes the importance of continued funding for such basic science, as it forms the foundation for future treatments. Public awareness is also key; lifestyle factors like smoking, poor diet, and lack of exercise contribute to heart disease, and preventing it remains the best strategy.

Critics and experts alike note that while promising, challenges remain. Ensuring that regenerated cells integrate properly without causing arrhythmias or tumors is crucial. Long-term studies will be needed to assess safety and efficacy. Nevertheless, the optimism is palpable. Patient advocacy groups, such as those supported by the BHF, have welcomed the news, with survivors sharing stories of how such advancements could change lives.

In the UK, where the National Health Service spends billions annually on heart disease management, regenerative therapies could alleviate economic burdens while saving lives. The collaboration between QMUL and UCL exemplifies the strength of interdisciplinary research, combining expertise in genetics, cardiology, and bioengineering.

As we look to the future, this study reminds us of the heart's hidden potential. What was once considered irreversible damage may soon be treatable through the body's own mechanisms. With ongoing support from organizations like the BHF, the dream of a self-healing heart edges closer to reality, offering hope to those affected by one of humanity's most pervasive health challenges.

This research not only advances scientific knowledge but also underscores the importance of investing in health innovation. As Dr. Rossi aptly put it, "The heart is more resilient than we thought; we just need to unlock its secrets." For now, the findings serve as a beacon of progress in the fight against heart disease, promising a healthier tomorrow for generations to come.

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Read the Full London Evening Standard Article at:
[ https://www.standard.co.uk/news/science/british-heart-foundation-queen-mary-university-of-london-university-college-london-b1240448.html ]