Document Detail


The telomere-telomerase axis and the heart.
MedLine Citation:
PMID:  17034355     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
Jan Kajstura; Marcello Rota; Konrad Urbanek; Toru Hosoda; Claudia Bearzi; Piero Anversa; Roberto Bolli; Annarosa Leri
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Antioxidants & redox signaling     Volume:  8     ISSN:  1523-0864     ISO Abbreviation:  Antioxid. Redox Signal.     Publication Date:    2006 Nov-Dec
Date Detail:
Created Date:  2006-10-12     Completed Date:  2007-01-30     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  100888899     Medline TA:  Antioxid Redox Signal     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2125-41     Citation Subset:  IM    
Affiliation:
Cardiovascular Research Institute, Department of Medicine, New York Medical College, Valhalla, New York 10595, USA. jan_kajstura@nymc.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiovascular Diseases / etiology,  metabolism*,  prevention & control
Cell Aging / physiology*
Homeostasis / physiology
Humans
Myocardium / enzymology,  metabolism*
Oxidative Stress / physiology*
Reactive Oxygen Species / metabolism
Telomerase / metabolism*
Telomere / physiology*
Grant Support
ID/Acronym/Agency:
AG-17042/AG/NIA NIH HHS; AG-23071/AG/NIA NIH HHS; AG-26107/AG/NIA NIH HHS; HL-38132/HL/NHLBI NIH HHS; HL-55757/HL/NHLBI NIH HHS; HL-65577/HL/NHLBI NIH HHS; HL-70897/HL/NHLBI NIH HHS; HL-75480/HL/NHLBI NIH HHS; HL-78825/HL/NHLBI NIH HHS; HL-81737/HL/NHLBI NIH HHS; HL65573/HL/NHLBI NIH HHS; HL68088/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species; EC 2.7.7.49/Telomerase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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