Depósito Académico >
CIMA (Centro de Investigación Médica Aplicada) >
Área de Ciencias Cardiovasculares >
Cardiopatía hipertensiva >
DA - CIMA - Cardiovasculares - Cardiopatía hipertensiva - Artículos de Revista >
|Telomere dysfunction in hypertension|
|Authors: ||Fuster, J.J. (José J.)|
Diez, J. (Javier)
Andres, V. (Vicente)
|Issue Date: ||2007|
|Publisher: ||Lippincott, Williams & Wilkins|
|Publisher version: ||http://bit.ly/IIJxoa|
|Citation: ||Fuster JJ, Diez J, Andres V. Telomere dysfunction in hypertension. J Hypertens 2007 Nov;25(11):2185-2192.|
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.
|Permanent link: ||http://hdl.handle.net/10171/21864|
|Appears in Collections:||DA - CIMA - Cardiovasculares - Cardiopatía hipertensiva - Artículos de Revista|
|Files in This Item:|
There are no files associated with this item.
Items in Dadun are protected by copyright, with all rights reserved, unless otherwise indicated.