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10.1007/s11926-018-0724-6 http://scihub22266oqcxt.onion/10.1007/s11926-018-0724-6 C5942182!5942182!29550994     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29550994.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Curr+Rheumatol+Rep 2018 ; 20 (4): 16 Nephropedia Template TP {{tp|p=29550994|t=2018. Sirtuins and Accelerated Aging in Scleroderma |pdf=|usr=}}{{29550994}} gab.com Text Sirtuins and Accelerated Aging in Scleroderma JO: Curr Rheumatol Rep http://www.kidney.de/pget.php?&tw=1&pmid=29550994 #FOAvip Purpose of Review: Premature activation of aging-associated molecular mechanisms is emerging as an important contributor to many diseases, including scleroderma. Among central regulators of the aging process are a group of histone deacetylases called sirtuins (SIRTs). Recent findings implicate these molecules as pathophysiological players in scleroderma skin and lung fibrosis. The goal of this article is to review recent studies on the involvement of SIRTs in scleroderma from the perspective of aging-related molecular mechanisms. Recent Findings: Despite a degree of controversy in this rapidly developing field, the majority of data suggest that SIRT levels are decreased in tissues from patients with scleroderma compared to healthy controls as well as in animal models of scleroderma. Molecular studies reveal several mechanisms through which declining SIRT levels contribute to fibrosis, with the most attention given to modulation of the TGF-? signaling pathway. Activation of SIRTs in cell culture and in animal models elicits antifibrotic effects. Summary: Declining SIRT levels and activity are emerging as pathophysiological contributors to scleroderma. Restoration of SIRTs may be therapeutic in patients with scleroderma. Twit Text FOAVip Sirtuins and Accelerated Aging in Scleroderma ????Curr Rheumatol Rep http://www.kidney.de/pget.php?&tw=1&pmid=29550994 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29550994 #FOAvip English Wikipedia <ref>{{Cite pmid|29550994}}</ref> Sirtuins and Accelerated Aging in Scleroderma #MMPMID29550994 Wyman AE; Atamas SP Curr Rheumatol Rep 2018[Mar]; 20 (4): 16 PMID29550994show ga Purpose of Review: Premature activation of aging-associated molecular mechanisms is emerging as an important contributor to many diseases, including scleroderma. Among central regulators of the aging process are a group of histone deacetylases called sirtuins (SIRTs). Recent findings implicate these molecules as pathophysiological players in scleroderma skin and lung fibrosis. The goal of this article is to review recent studies on the involvement of SIRTs in scleroderma from the perspective of aging-related molecular mechanisms. Recent Findings: Despite a degree of controversy in this rapidly developing field, the majority of data suggest that SIRT levels are decreased in tissues from patients with scleroderma compared to healthy controls as well as in animal models of scleroderma. Molecular studies reveal several mechanisms through which declining SIRT levels contribute to fibrosis, with the most attention given to modulation of the TGF-? signaling pathway. Activation of SIRTs in cell culture and in animal models elicits antifibrotic effects. Summary: Declining SIRT levels and activity are emerging as pathophysiological contributors to scleroderma. Restoration of SIRTs may be therapeutic in patients with scleroderma. äSirtuins and Accelerated Aging in Scleroderma (epmc).pdf DeepDyve Pubget Overpricing