Nazar Labinskyy

TL;DR: It is found that resveratrol treatment has a range of beneficial effects in mice but does not increase the longevity of ad libitum-fed animals when started midlife.

TL;DR: It is proposed that SIRT1, via a pathway that involves the upregulation of eNOS, induces mitochondrial biogenesis in endothelial cells via activating SIRT 1, and the potential for new treatment approaches targeting endothelial mitochondria in metabolic diseases is suggested.

TL;DR: In this paper, the authors investigated the effect of resveratrol on mtROS production in cultured human coronary arterial endothelial cells (CAECs) and found that reserveratrol attenuates both steady-state and high glucose (30 mM)-induced mtRos production in CAECs, an effect that was prevented by the knockdown of the protein deacetylase silent information regulator 2/sirtuin 1 (SIRT1), an intracellular target of reserver atrin 1.

TL;DR: Increased mitochondrial oxidative stress contributes to endothelial NF-kappaB activation, which contributes to the pro-inflammatory phenotypic alterations in the aged vaculature, and the model predicts that by reducing mitochondrial H(2)O( 2) production and/or directly inhibiting NF- kappaB novel anti-aging pharmacological treatments will exert significant anti-inflammatory and vasoprotective effects.

TL;DR: A large number of studies suggest that Mediterranean diets rich in resveratrol are associated with reduced risk of coronary artery disease, but the mechanisms by which this association is driven are still poorly understood.