Related Experiment Video

Updated: Feb 13, 2026

Deacetylation Assays to Unravel the Interplay between Sirtuins SIRT2 and Specific Protein-substrates
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Deacetylation Assays to Unravel the Interplay between Sirtuins SIRT2 and Specific Protein-substrates

Published on: February 27, 2016

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Sirtuins and Accelerated Aging in Scleroderma

Anne E Wyman1,2,3, Sergei P Atamas4,5

  • 1Geriatric Research Education and Clinical Center (GRECC), VA Maryland Health Care Center, Baltimore VA Medical Center, Baltimore, MD, USA.

Current Rheumatology Reports
|March 19, 2018
PubMed
Abstract

Insights

Scleroderma is linked to aging mechanisms and reduced sirtuin (SIRT) levels. Restoring SIRT activity shows promise for treating fibrosis in scleroderma patients.

Area of Science:

  • Molecular Biology
  • Aging Research
  • Rheumatology

Background:

  • Aging processes contribute to diseases like scleroderma.
  • Sirtuins (SIRTs) are key regulators of aging.
  • SIRTs are implicated in scleroderma pathogenesis, particularly fibrosis.

Purpose of the Study:

  • To review the role of SIRTs in scleroderma.
  • To examine SIRT involvement through the lens of aging-related mechanisms.

Main Methods:

  • Literature review of recent studies on SIRTs and scleroderma.
  • Analysis of molecular mechanisms linking SIRTs to fibrosis.
  • Examination of SIRT modulation in cellular and animal models.

Main Results:

  • SIRT levels are generally decreased in scleroderma patients and models.
  • Reduced SIRTs contribute to fibrosis, notably via TGF-β signaling.
  • Activating SIRTs demonstrates antifibrotic effects in experimental settings.

Conclusions:

  • Declining SIRT levels and activity are pathophysiological factors in scleroderma.
  • Restoration of SIRT function may offer a therapeutic strategy for scleroderma.
Keywords:
AgingFibroblastFibrosisLungSIRTSScSclerodermaSirtuinSkinSystemic sclerosis

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