By José Marín-García M.D., Michael J. Goldenthal, Gordon W. Moe (auth.)
Cardiac getting older, like getting older commonly, is a posh strategy. quite a few mobile and molecular alterations give a contribution to the expression of the a number of phenotypes of getting older, "the various faces" of cardiac getting older. during this ebook, the genetic and molecular foundation of cardiovascular getting older might be mentioned. additionally, a finished evaluation of the bioenergetic adjustments that ensue in human and animal types of cardiac getting older in addition to present diagnostic and destiny healing modalities could be undertaken.
José Marín-García is Director, The Molecular Cardiology and Neuromuscular Institute, Highland Park, New Jersey.
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Temperature drop in winter) than by lethal ones. ). In particular one of them, hypergravity decreases the rate of behavioral aging. At this time the mechanisms whereby these stresses increase longevity are not clear, although they may involve metabolic regulation and induction of stress protein such as heat shock proteins (HSPs). It is worth noting than in response to increased level of ROS in the senescent heart, genes encoding mitochondrial stress proteins including both heat shock and antioxidant response proteins, such as HSP60, HO-1 and GPx are up-regulated .
Elephants), such as increasing knowledge, leadership, well being, relationships and creativity. References 1. Luciani F, Valensin S, Vescovini R, Sansoni P, Fagnoni F, Franceschi C, Bonafe M, Turchetti G. A stochastic model for CD8(+)T cell dynamics in human immunosenescence: implications for survival and longevity. J Theor Biol 2001;213:587–597 2. De Benedictis G, Tan Q, Jeune B, Christensen K, Ukraintseva SV, Bonafe M, Franceschi C, Vaupel JW, Yashin AI. Recent advances in human gene-longevity association studies.
H2 O2 production and oxidative damage) and increased genomic stability as indicated by reduced levels of mtDNA deletions in both heart and skeletal muscle. The observation that a relatively large increase in life span results from the up-regulation of a single gene involved in boosting antioxidant defenses, and its targeting to the mitochondria, buttresses the notion that mitochondrial ROS and OS play a critical role in determining life span, and are to date the most compelling support for FRTA.