Telomere dysfunction in hypertension

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Abstract
8 páginas, 2 figuras.-- El documento en word es la versión post-print.Aging is a major risk factor for hypertension and associated cardiovascular disease. In most proliferative tissues, aging is characterized by shortening of the DNA component of telomeres, the specialized genetic segments that cap the end of eukaryotic chromosomes and protect them from end-to-end fusions. By inducing genomic instability, replicative senescence and apoptosis, telomere shortening is thought to contribute to organismal aging and to the development of age-related diseases. Here, we review animal and human studies that have investigated the possible links between telomere ablation and the pathogenesis of hypertension and related target organ damage. Although evidence is mounting that alterations in telomerase activity and telomere shortening may play a role in the pathogenesis of hypertension, additional studies are required to understand the molecular mechanisms by which telomere dysfunction and hypertension are functionally connected. As our knowledge on this emerging field grows, the challenge will be to ascertain whether all this information might translate into clinical applications.Work in the author’s laboratories is partly supported by\ud grants from Ministerio de Sanidad y Consumo, Instituto\ud de Salud Carlos III (Red Temática de Investigación\ud Cooperativa Cardiovascular RECAVA), and from the\ud Ministerio de Educación y Ciencia and the European\ud Regional Development Fund (SAF2004-03057). J.J.F. is\ud supported by a CSIC-I3P predoctoral fellowship co-sponsored\ud by the European Social Fund.Peer reviewe