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2018 ; 20
(4
): 16
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Sirtuins and Accelerated Aging in Scleroderma
#MMPMID29550994
Wyman AE
; Atamas SP
Curr Rheumatol Rep
2018[Mar]; 20
(4
): 16
PMID29550994
show 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. Declining SIRT levels and activity are
emerging as pathophysiological contributors to scleroderma. Restoration of SIRTs
may be therapeutic in patients with scleroderma.
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