title: The telomere-telomerase axis and the heart.
abstract: The preservation of myocyte number and cardiac mass throughout life is dependent on the balance between cell death and cell division. Rapidly emerging evidence indicates that new myocytes can be formed through the activation and differentiation of resident cardiac progenitor cells. The critical issue is the identification of mechanisms that define the aging of cardiac progenitor cells and, ultimately, their inability to replace dying myocytes. The most reliable marker of cellular senescence is the modification of the telomere-telomerase axis, together with the expression of the cell cycle inhibitors p16INK4a and p53. Cellular senescence is characterized by biochemical events that occur within the cell. In this regard, one of the most relevant processes is represented by repeated oxidative stress that may evolve into the activation of the cell death program or result in the development of a senescent phenotype. Thus, the modulation of telomerase activity and the control of telomeric length, together with the attenuation of the formation of reactive oxygen species, may represent important therapeutic tools in regenerative medicine and in prevention of aging and diabetic cardiomyopathies.
authors.affiliation: Cardiovascular Research Institute, Department of Medicine, New York Medical College, Valhalla, New York 10595, USA. jan_kajstura@nymc.edu
authors.forename: Jan
authors.initials: J
authors.lastname: Kajstura
authors.forename: Marcello
authors.initials: M
authors.lastname: Rota
authors.forename: Konrad
authors.initials: K
authors.lastname: Urbanek
authors.forename: Toru
authors.initials: T
authors.lastname: Hosoda
authors.forename: Claudia
authors.initials: C
authors.lastname: Bearzi
authors.forename: Piero
authors.initials: P
authors.lastname: Anversa
authors.forename: Roberto
authors.initials: R
authors.lastname: Bolli
authors.forename: Annarosa
authors.initials: A
authors.lastname: Leri
mesh_terms: D000818:Animals; D002318:Cardiovascular Diseases / Q000209:etiology / Q000378:metabolism* / Q000517:prevention & control; D016922:Cellular Senescence / Q000502:physiology*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D019098:Telomerase / Q000378:metabolism*; D016615:Telomere / Q000502:physiology*
chemical_list: D017382:Reactive Oxygen Species; D019098:Telomerase