Aging and the Heart: A Post-Genomic View by José Marín-García M.D., Michael J. Goldenthal, Gordon W. Moe

By José Marín-García M.D., Michael J. Goldenthal, Gordon W. Moe (auth.)

Cardiac getting older, like getting older more often than not, is a posh procedure. a variety of mobile and molecular adjustments give a contribution to the expression of the a number of phenotypes of getting older, "the diverse faces" of cardiac getting older. during this publication, the genetic and molecular foundation of cardiovascular getting older might be mentioned. moreover, a finished evaluation of the bioenergetic alterations that take place in human and animal versions of cardiac getting older in addition to present diagnostic and destiny healing modalities can be undertaken.

José Marín-García is Director, The Molecular Cardiology and Neuromuscular Institute, Highland Park, New Jersey.

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They are extremely reactive compounds that will come to have a new electron in any way possible. In this process, the free radical will attach itself to another molecule modifying it biochemically. As FRs steal an electron from other molecules, they may convert these molecules into de novo FRs, or break down or alter their chemical structure. These aggressive compounds induce damage to cellular macromolecules such as DNA, lipids and proteins. The main FRs and non-FRs mimics are called reactive oxygen species” or ROS, including superoxide radical (SOR), hydroxyl radical (OHR), hydroperoxyl radical (HPR), alkoxyl radical (AR), peroxyl radical (PR) and nitric oxide radical (NOR).

F) The Hayflick Theory The central premise of this theory relates to findings that human somatic cells are limited in the number of times that they can divide, and suggests that to live longer there is a need to slow down the rate of cell division. Changes in cell proliferation could be accomplished by a number of changes, including dietary (see Chapter 15 on CR) and lifestyle as well as well as by invoking signaling elements of senescence pathways. Interestingly, both growth factors and OS can modulate cell proliferation.

Von Zglinicki T, Martin-Ruiz CM. Telomeres as biomarkers for ageing and age-related diseases. Curr Mol Med 2005;5:197–203 92. Martin-Ruiz CM, Gussekloo J, van Heemst D, von Zglinicki T, Westendorp RG. Telomere length in white blood cells is not associated with morbidity or mortality in the oldest old: a population-based study. Aging Cell 2005;4:287–289 93. Collerton J, Martin-Ruiz C, Kenny A, Barrass K, von Zglinicki T, Kirkwood T, Keavney B. Telomere length is associated with left ventricular function in the oldest old: the Newcastle 85+ study.

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Aging and the Heart: A Post-Genomic View by José Marín-García M.D., Michael J. Goldenthal, Gordon W. Moe
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