Aging, telomeres and heart failure.
During normal aging, the heart undergoes functional, morphological and cellular changes. Although aging per se does not lead to the expression of heart failure, it is likely that age-associated changes lower the threshold for the manifestation of signs and symptoms of heart failure. In patients, the susceptibility, age of onset and pace of progression of heart failure are highly variable. The presence of conventional risk factors cannot completely explain this variability. Accumulation of DNA damage and telomere attrition results in an increase in cellular senescence and apoptosis, resulting in a decrease in the number and function of cells, contributing to the overall tissue and organ dysfunction. Biological aging, characterized by reduced telomere length, provides an explanation for the highly interindividual variable threshold to express the clinical syndrome of heart failure at some stage during life. In this review, we will elaborate on the current knowledge of aging of the heart, telomere biology and its potential role in the development of heart failure.
Division of Experimental Cardiology, Department of Cardiology, University Medical Center Groningen, University of Groningen, Hanzeplein 1, 9700 RB Groningen, The Netherlands.
Liza S M
LS
Wong
Pim
P
van der Harst
Rudolf A
RA
de Boer
Jardi
J
Huzen
Wiek H
WH
van Gilst
Dirk J
DJ
van Veldhuisen
D000375:Aging / Q000473:pathology*; D018450:Disease Progression; D006333:Heart Failure / Q000201:enzymology* / Q000235:genetics; D006801:Humans; D032383:Myocytes, Cardiac / Q000201:enzymology; D011379:Prognosis; D012307:Risk Factors; D019098:Telomerase / Q000235:genetics* / Q000378:metabolism; D016615:Telomere / Q000201:enzymology / Q000235:genetics*
D019098:Telomerase