Open AccessRole of Cellular Senescence in Lifestyle-Related Disease
Author(s) -
Tohru Minamino
Publication year - 2010
Publication title -
circulation journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.949
H-Index - 106
eISSN - 1347-4820
pISSN - 1346-9843
DOI - 10.1253/circj.cj-10-0916
Subject(s) - senescence , telomere , disease , biology , cellular senescence , phenotype , diabetes mellitus , mechanism (biology) , cellular aging , longevity , dna repair , genetics , type 2 diabetes , bioinformatics , gerontology , medicine , gene , endocrinology , philosophy , epistemology
Epidemiological studies have shown that age is the chief risk factor for lifestyle-related diseases such as cardiovascular disease and diabetes, but the molecular mechanisms that underlie the increase in the risk of such diseases conferred by aging remain unclear. Recently, genetic analyses using various animal models have identified molecules that are crucial for aging. These include components of the DNA repair system, the tumor suppressor pathway, the telomere maintenance system, the insulin/Akt pathway, and other metabolic pathways. Interestingly, most of the molecules that influence the phenotypic changes of aging also regulate cellular senescence, suggesting a causative link between cellular senescence and aging. This review examines the hypothesis that cellular senescence might contribute to lifestyle-related disease.