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

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