Defective DNA-damage repair induced by nuclear lamina dysfunction is a key mediator of smooth muscle cell aging

Warren, Derek T. and Shanahan, Catherine M. (2011) Defective DNA-damage repair induced by nuclear lamina dysfunction is a key mediator of smooth muscle cell aging. Biochemical Society Transactions, 39 (6). pp. 1780-1785. ISSN 0300-5127

Full text not available from this repository. (Request a copy)

Abstract

Accumulation of DNA damage is a major driving force of normal cellular aging and has recently been demonstrated to hasten the development of vascular diseases such as atherosclerosis. VSMCs (vascular smooth muscle cells) are essential for vessel wall integrity and repair, and maintenance of their proliferative capacity is essential for vascular health. The signalling pathways that determine VSMC aging remain poorly defined; however, recent evidence implicates persistent DNA damage and the A-type nuclear lamins as key regulators of this process. In the present review, we discuss the importance of the nuclear lamina in the spatial organization of nuclear signalling events, including the DNA-damage response. In particular, we focus on the evidence suggesting that prelamin A accumulation interferes with nuclear spatial compartmentalization by disrupting chromatin organization and DNA-damage repair pathways to promote VSMC aging and senescence.

Item Type: Article
Uncontrolled Keywords: aging,dna-damage repair,nuclear lamina,persistent dna damage,smooth muscle cell
Faculty \ School: Faculty of Science > School of Pharmacy
Related URLs:
Depositing User: Pure Connector
Date Deposited: 23 Nov 2016 00:42
Last Modified: 22 Apr 2020 01:57
URI: https://ueaeprints.uea.ac.uk/id/eprint/61456
DOI: 10.1042/BST20110703

Actions (login required)

View Item View Item