Activation of Cardiac Progenitor Cells Reverses the Failing Heart Senescent Phenotype and Prolongs Lifespan

• DOI: 10.1161/circresaha.107.165464
• Publication Date: 2008-01-18T02:06:56Z
• Authors: Arantxa Gonzalez; Marcello Rota; Daria Nurzynska; Yu Misao; Jochen Tillmanns; Caroline Ojaimi; M. Elena Padin-Ir...; Patrick Müller; Grazia Esposito; Claudia Bearzi; Serena Vitale; Buddhadeb Dawn; Santosh K. Sangan...; Mathue Baker; Thomas H. Hintze; Roberto Bolli; Konrad Urbanek; Toru Hosoda; Piero Anversa; Jan Kajstura; Annarosa Leri
• Keywords: Senescence

Heart failure is the leading cause of death in elderly, but whether this result a primary aging myopathy dictated by depletion cardiac progenitor cell (CPC) pool unknown. Similarly, current lifespan reflects ineluctable genetic clock or heart interferes with genetically determined fate organ and organism an important question. We have identified that chronological age leads to telomeric shortening CPCs, which necessity generate differentiated progeny rapidly acquires senescent phenotype conditioning aging. CPC mediated attenuation insulin-like growth factor-1/insulin-like factor-1 receptor hepatocyte factor/c-Met systems, do not counteract any longer renin-angiotensin system, resulting cellular senescence, arrest, apoptosis. However, pulse-chase 5-bromodeoxyuridine-labeling assay revealed contains functionally competent CPCs properties stem cells. This subset telomerase-competent long telomeres and, following activation, migrate regions damage, where they population young cardiomyocytes, reversing partly myopathy. The are corrected some extent, prolongation maximum lifespan.