In the July issue of the Journal of Molecular and Cellular Cardiology, the official publication of the International Society for Heart Research, researchers demonstrated for the first time that pretreatment with a clinically relevant dose of rapamycin induces a protective effect against heart attack injury and reduces programmed cell death.
Researchers believe through the opening of the mitochondrial KATP channel of heart cells, rapamycin enables cells to maintain ATP levels. Mitochondria are cellular organelles critical for converting oxygen into ATP, the key fuel for cellular function.
"Rapamycin may one day be beneficial as a potential therapeutic strategy to limit cell death caused by ischemia or reperfusion injury, and possibly long-term prevention of ventricular remodeling ?the changes in size, shape and function that may occur to the left ventricle of the heart," said Rakesh C. Kukreja, Ph.D., professor of medicine and Eric Lipman Chair of Cardiology at VCU. Kukreja is lead author of the study.
Rapamycin blocks protein synthesis by inhibiting the mammalian target of rapamycin (mTOR), an essential component in the pathway of the cell cycle progression. The drug has been found to be important in transplant medicine and especially in kidney or heart transplantation. Additionally, Kukreja said that because of the antibiotic's antigrowth properties, rapamycin effectively reduces coronary restonosis, the abnormal narrowing of a blood vessel. In coronary angioplasty, stents coated with rapamycin are implanted to reduce the risk of restonosis.
"A significant clinical question will be whether or not rapamycin coated stents can be utilized in patients to favorably affect damaged heart muscle beyond the
Source:Virginia Commonwealth University