A new study in swine (pigs) has found that sermorelin can reduce scarring of heart muscle after a heart attack. This information confirms previous findings from research in rat models of heart attack. In the future, sermorelin and other GHRH agonists may be useful for treating post-infarction (after a heart attack) patients. These peptides have the potential to reduce long-term damage, speed recovery, and reduce complication rates.
The Scale of the Problem
Survival following a heart attack has improved with advances in care, but damage to the heart muscle often leads to a weakened pump function and heart failure. This is a serious condition, as 50% of individuals die within 5 years of a diagnosis of heart failure1. Clearly, reducing long-term consequences of a heart attack can improve survival. It can also improve morbidity as heart failure is an extremely debilitating condition.
The immediate damage caused by a heart attack is only one part of a larger problem that eventually leads to fatal heart failure. Other components of the problem include scar formation as well as generalized inflammation. Scar formation occurs secondary to wound healing. It can weaken the walls of the heart and interfere with the normal conduction of electrical signals. Post-infarction inflammation can weaken both the mechanical structure and electrical functioning of the heart as well. Without proper muscle structure, the heart cannot contract with enough force. Without proper electrical functioning, contractions are not coordinated or efficient and flow becomes turbulent. The ability to reduce inflammation and cardiac remodeling could drastically reduce the long-term consequences of heart attack2.
The Role of GHRH Agonists in Myocardial Repair
The current management of heart failure aims to maximize the effectiveness of whatever heart function remains. Unfortunately, morbidity and mortality remain high because the heart, in its weakened state, is more vulnerable to the effects of aging. New therapies aim to prevent remodeling, the change in heart structure that occurs secondary to scar formation and inflammation and which ultimately makes the heart weaker and less able to withstand the effects of aging.
Previous studies of rat heart tissue found that cardiomyocytes (heart cells) express GHRH receptors on their surfaces. Laboratory studies have since shown that cardiomyocytes survive in greater numbers, after being starved of oxygen, when a GHRH agonist is provided in addition to standard nutrients. This suggests that heart cells might also survive better following a heart attack if a GHRH agonist is administered. As it turns out, GHRH affects the survival of cardiomyocytes in several ways including
- Reducing the expression of genes associated with cell death (apoptosis),
- Increasing the expression of genes associated with extracellular matrix synthesis,
- Increasing the growth of capillaries needed to supply oxygen-rich blood to damaged cells, and
- Reducing the production of pro-inflammatory substances2.
Research has shown that the administration of a GHRH antagonist (blocker) reverses all of the positive benefits of a GHRH agonist3. This research further indicates that it is GHRH that is responsible for reducing cardiac remodeling and improving cell survival. In short, GHRH can act directly on cardiomyocytes to keep them healthy and functioning properly, even after damage due to a heart attack.
Sermorelin and Pig Heart Muscle
Rats are reasonable models for early experiments because they are easy to work with and a great deal is known about their physiology. Unfortunately, rats are not all that similar to humans and so any findings based on rat models must be treated with a degree of skepticism until replicated in another species. Pigs, in particular, offer an attractive alternative because their physiology is similar to that of humans.
When sermorelin was administered to pigs who had undergone simulated heart attacks, the pig hearts demonstrated smaller scars, increased capillary growth, and improved diastolic (relaxation phase) heart function2. Overall, these results suggest that GHRH agonists like sermorelin may one day play an integral role in post-heart attack care and recovery.
Sermorelin is still undergoing scientific research studies and is not yet approved for human use by the FDA. You can find out more about sermorelin at peptidesciences.com.
- Kanashiro-Takeuchi, R. M. et al. New therapeutic approach to heart failure due to myocardial infarction based on targeting growth hormone-releasing hormone receptor. Oncotarget 6, 9728–9739 (2015).
- Bagno, L. L. et al. Growth Hormone–Releasing Hormone Agonists Reduce Myocardial Infarct Scar in Swine With Subacute Ischemic Cardiomyopathy. J. Am. Heart Assoc. Cardiovasc. Cerebrovasc. Dis. 4, (2015).
3. Granata, R. et al. Growth hormone-releasing hormone promotes survival of cardiac myocytes in vitro and protects against ischaemia–reperfusion injury in rat heart. Cardiovasc. Res. 83, 303–312 (2009).