The telomere-telomerase axis and the heart

Jan Kajstura, Marcello Rota, Konrad Urbanek, Toru Hosoda, Claudia Bearzi, Piero Anversa, Roberto Bolli, Annarosa Leri

Research output: Contribution to journalArticlepeer-review

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 p16 INK4a 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.

Original languageEnglish
Pages (from-to)2125-2141
Number of pages17
JournalAntioxidants and Redox Signaling
Volume8
Issue number11-12
Publication statusPublished - Nov 2006

ASJC Scopus subject areas

  • Biochemistry

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