New Understanding of the Biology of Senescent Cells in Hearts Could Lead to Antiaging Progress

Newcastle University researchers are exploring the effects of removing senescent cells that form as a result of a heart attack.

Heart cells, cardiomyocytes, rarely divide it was not known how these cells could become senescent. Senescent cells are also called zombie cells. Zombie cells do not function correctly and can cause other cells around them to become senescent.

The Newcastle scientists, in collaboration with researchers in the US and France, have discovered how senescence occurs in the heart and how it might be reversed or treated.

There are already many companies and academic researchers working on the treatment of senescent cells.

Unity Biotechnologies is a publicly traded company with a current valuation of about $485 million. Unity Biotechnology is developing drugs which target senescent cells. They have clinical trials for the treatment of arthritis and macular degeneration. They are selecting and testing candidate drugs for treating heart disease that is caused by senescent cells.

There are over a dozen other companies working on the treatment of senescent cells.

The EMDO Journal – Length‐independent telomere damage drives post‐mitotic cardiomyocyte senescence

Abstract – Length‐independent telomere damage drives post‐mitotic cardiomyocyte senescence

Aging is the biggest risk factor for cardiovascular disease. Cellular senescence, a process driven in part by telomere shortening, has been implicated in age‐related tissue dysfunction. Here, we address the question of how senescence is induced in rarely dividing/post‐mitotic cardiomyocytes and investigate whether clearance of senescent cells attenuates age‐related cardiac dysfunction. During aging, human and murine cardiomyocytes acquire a senescent‐like phenotype characterized by persistent DNA damage at telomere regions that can be driven by mitochondrial dysfunction and crucially can occur independently of cell division and telomere length. Length‐independent telomere damage in cardiomyocytes activates the classical senescence‐inducing pathways, p21CIP and p16INK4a, and results in a non‐canonical senescence‐associated secretory phenotype, which is pro‐fibrotic and pro‐hypertrophic. Pharmacological or genetic clearance of senescent cells in mice alleviates detrimental features of cardiac aging, including myocardial hypertrophy and fibrosis. Our data describe a mechanism by which senescence can occur and contribute to age‐related myocardial dysfunction and in the wider setting to aging in post‐mitotic tissues.

Written by Christina Wong

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