Evidence map›Paper›PMID 28800254›Full record

ArticleAmerican journal of respiratory cell and molecular biology2018

Sirtuin1 Protects against Systemic Sclerosis-related Pulmonary Fibrosis by Decreasing Proinflammatory and Profibrotic Processes.

Haiyan Chu, Shuai Jiang, Qingmei Liu, Yanyun Ma, Xiaoxia Zhu, Minrui Liang, Xiangguang Shi, Weifeng Ding, Xiaodong Zhou, Hejian Zou and 4 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.7field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

45 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. SIRT3/6/7: promising therapeutic targets for pulmonary fibrosis.Frontiers in cell and developmental biology · 2025
    Review
  6. Role of epigenetics in corneal health and disease.Progress in retinal and eye research · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. The Molecular Mechanisms of Systemic Sclerosis-Associated Lung Fibrosis.International journal of molecular sciences · 2023
    Review
  18. Epigenetic Dysregulation in Autoimmune and Inflammatory Skin Diseases.Clinical reviews in allergy & immunology · 2022
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 7 institutions in 4 countries.

Haiyan Chu1 State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences.
Shuai Jiang1 State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences.
Qingmei Liu1 State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences.
Yanyun Ma3 Ministry of Education Key Laboratory of Contemporary Anthropology, School of Life Sciences.
Xiaoxia Zhu4 Division of Rheumatology, Shanghai Medical College and Huashan Hospital, and.
Minrui Liang4 Division of Rheumatology, Shanghai Medical College and Huashan Hospital, and.
Xiangguang Shi1 State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences.
Weifeng Ding1 State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences.
Xiaodong Zhou7 University of Texas-McGovern Medical School, Houston, Texas; and.
Hejian Zou4 Division of Rheumatology, Shanghai Medical College and Huashan Hospital, and.
Feng Qian3 Ministry of Education Key Laboratory of Contemporary Anthropology, School of Life Sciences.
Philip W Shaul8 Center for Pulmonary and Vascular Biology, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas.
Li Jin1 State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences.
Jiucun Wang1 State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences.
State Key Laboratory of Genetic EngineeringFudan University · CNHuashan Hospital · CNInstitute of Contemporary History · SIInstitut thématique Génétique, génomique et bioinformatique · FRThe University of Texas Health Science Center · USThe University of Texas Southwestern Medical Center · US

Funding

Studies of HLA Region Genomics in Systemic Sclerosis and Ankylosing SpondyilitisU01AI090909 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MAYES, MAUREEN MAUREEN, REVEILLE, JOHN DUFFIN · 2010 to 2014
$2.9M
NIAID NIH HHS U01 AI090909
6 · The paper itself

Abstract

Pulmonary fibrosis is the leading cause of death in systemic sclerosis (SSc). Sirtuin1 (SIRT1) is a deacetylase with known antiinflammatory and antifibrotic activity in the liver, kidney, and skin. The role of SIRT1 in SSc-related pulmonary fibrosis is unknown. In the present work, we determined that the expression of SIRT1 in peripheral blood mononuclear cells of patients with SSc with pulmonary fibrosis is lower than that in patients with SSc without pulmonary fibrosis. In in vivo studies of bleomycin-induced lung fibrosis in mice, SIRT1 activation with resveratrol reduced collagen production when it was administered either prophylactically during the inflammatory stage or after the development of fibrosis. Furthermore, SIRT1 activation or overexpression inhibited tumor necrosis factor-α-induced inflammatory responses in vitro in human fetal lung fibroblasts, depletion of SIRT1 in fibroblasts enhanced inflammation, and these effects were related to changes in the acetylation of NF-κB. In addition, SIRT1 activation or exogenous overexpression inhibited collagen production in vitro, and these manipulations also inhibited fibrosis via inactivation of transforming growth factor-β/mothers against decapentaplegic homolog and mammalian target of rapamycin signaling. Taken together, our results show that a loss of SIRT1 may participate in the pathogenesis of SSc-related pulmonary fibrosis, and that SIRT1 activation is an effective treatment for both the early (inflammatory) and late (fibrotic) stages of pulmonary fibrosis. Thus, SIRT1 may be a promising therapeutic target in the management of SSc-related pulmonary fibrosis.

Indexed as

Pulmonary FibrosisScleroderma, SystemicAnimalsCell LineEnzyme ActivationFemaleHumansMaleMiceNF-kappa BSirtuin 1Tumor Necrosis Factor-alphaNF-kappa BSIRT1 protein, humanSirt1 protein, mouseSirtuin 1Tumor Necrosis Factor-alphainflammationNF-κB pathwaypulmonary fibrosissystemic sclerosistransforming growth factor-β/mammalian target of rapamycin pathway

Identifiers

PMID28800254
PMCPMC5941307
OpenAlexW2743970793

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.