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Download the Issue @ a Glance podcast Subscribe to the EHJ Podcast !Graphic1 With the impressive increase in life expectancy due to improved nutrition, hygiene, and modern medicine,1 chronic diseases such as atherosclerosis,2 diseases of the bones and joints,3 as well as degenerative diseases of the central nervous system4 have become increasingly prevalent. Most of these chronic diseases are highly age dependent.5 As Western societies are ageing due to an increased life span, decreased birth rates, and improving social and health conditions, age as a facilitator or cause of chronic diseases came into focus. Of note, as outlined in the Clinical Review entitled ‘ Molecular mechanism of endothelial and vascular ageing: implications for cardiovascular disease ’, by Giovanni G. Camici and colleagues from the University of Zurich in Switzerland,6 ageing is mediated by distinct molecular processes that can be characterized as thoroughly as those causing cardiovascular disease. Indeed, it is well known that oxidative stress produced in the mitochondria and cytosol of the heart and brain contributes to ageing of the organs. The mitochondrial adaptor protein p66Shc, transcription factors such as junD, and sirtuins regulate the ageing process, determine the life span of many species, and are involved in cardiovascular diseases. GDF11, a member of the transforming growth factor β (TGFβ) superfamily with homology to myostatin has also been suggested to retard ageing via as yet unknown mechanisms, although this has recently been challenged by some,7 but not others.8 Finally, telomere length is involved in ageing and age-related cardiovascular dysfunction.9 The second Clinical Review , entitled ‘Protective effects of sirtuins in cardiovascular diseases: from bench to bedside ’,10 by Christian M. Matter also from the University Hospital Zurich, Switzerland continues along these lines, but focuses specifically on the cardiovascular … 1: /embed/inline-graphic-1.gif
Thomas F. Lüscher (Mon,) studied this question.