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Potential mechanisms linking atherosclerosis and increased cardiovascular risk in COPD: focus on Sirtuins.

Abstract：

:The development of atherosclerosis is a multi-step process, at least in part controlled by the vascular endothelium function. Observations in humans and experimental models of atherosclerosis have identified monocyte recruitment as an early event in atherogenesis. Chronic inflammation is associated with ageing and its related diseases (e.g., atherosclerosis and chronic obstructive pulmonary disease). Recently it has been discovered that Sirtuins (NAD+-dependent deacetylases) represent a pivotal regulator of longevity and health. They appear to have a prominent role in vascular biology and regulate aspects of age-dependent atherosclerosis. Many studies demonstrate that SIRT1 exhibits anti-inflammatory properties in vitro (e.g., fatty acid-induced inflammation), in vivo (e.g., atherosclerosis, sustainment of normal immune function in knock-out mice) and in clinical studies (e.g., patients with chronic obstructive pulmonary disease). Because of a significant reduction of SIRT1 in rodent lungs exposed to cigarette smoke and in lungs of patients with chronic obstructive pulmonary disease (COPD), activation of SIRT1 may be a potential target for chronic obstructive pulmonary disease therapy. We review the inflammatory mechanisms involved in COPD-CVD coexistence and the potential role of SIRT1 in the regulation of these systems.

journal_name

Int J Mol Sci

journal_title

International journal of molecular sciences

authors

Corbi G,Bianco A,Turchiarelli V,Cellurale M,Fatica F,Daniele A,Mazzarella G,Ferrara N

doi

10.3390/ijms140612696

subject

Has Abstract

pub_date

2013-06-17 00:00:00

pages

12696-713

issue

6

issn

1422-0067

pii

ijms140612696

journal_volume

14

pub_type

杂志文章,评审

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