Evidence map›Paper›PMID 37777567›Full record

ArticleCell death & disease2023

SIRT2 alleviated renal fibrosis by deacetylating SMAD2 and SMAD3 in renal tubular epithelial cells.

Shu Yang, Guangyan Yang, Xinyu Wang, Jiaqing Xiang, Lin Kang, Zhen Liang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  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

6 authors at 2 institutions in 1 country.

Shu Yang *Department of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University & The First Affiliated Hospital of Southern University of Science and Technology), Shenzhen, China. yang.shu@szhospital.com.ORCID 0000-0002-4912-777X
Guangyan Yang *Department of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University & The First Affiliated Hospital of Southern University of Science and Technology), Shenzhen, China.ORCID 0000-0003-4498-5844
Xinyu Wang *Department of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University & The First Affiliated Hospital of Southern University of Science and Technology), Shenzhen, China.
Jiaqing XiangDepartment of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University & The First Affiliated Hospital of Southern University of Science and Technology), Shenzhen, China.
Lin KangDepartment of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University & The First Affiliated Hospital of Southern University of Science and Technology), Shenzhen, China. kang.lin@szhospital.com.ORCID 0009-0006-2986-797X
Zhen LiangDepartment of Geriatrics, Shenzhen People's Hospital (The Second Clinical Medical College of Jinan University & The First Affiliated Hospital of Southern University of Science and Technology), Shenzhen, China. liang.zhen@szhospital.com.ORCID 0000-0003-4700-0203
Jinan University · CNSouthern University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transforming growth factor-β (TGF-β) is the primary factor that drives fibrosis in most, if not all, forms of chronic kidney disease. In kidneys that are obstructed, specific deletion of Sirt2 in renal tubule epithelial cells (TEC) has been shown to aggravate renal fibrosis, while renal tubule specific overexpression of Sirt2 has been shown to ameliorate renal fibrosis. Similarly, specific deletion of Sirt2 in hepatocyte aggravated CCl4-induced hepatic fibrosis. In addition, we have demonstrated that SIRT2 overexpression and knockdown restrain and enhance TGF-β-induced fibrotic gene expression, respectively, in TEC. Mechanistically, SIRT2 reduced the phosphorylation, acetylation, and nuclear localization levels of SMAD2 and SMAD3, leading to inhibition of the TGF-β signaling pathway. Further studies have revealed that that SIRT2 was able to directly interact with and deacetylate SMAD2 at lysine 451, promoting its ubiquitination and degradation. Notably, loss of SMAD specific E3 ubiquitin protein ligase 2 abolishes the ubiquitination and degradation of SMAD2 induced by SIRT2 in SMAD2. Regarding SMAD3, we have found that SIRT2 interact with and deacetylates SMAD3 at lysine 341 and 378 only in the presence of TGF-β, thereby reducing its activation. This study provides initial indication of the anti-fibrotic role of SIRT2 in renal tubules and hepatocytes, suggesting its therapeutic potential for fibrosis.

Indexed as

LysineRenal Insufficiency, ChronicEpithelial CellsFibrosisHumansSirtuin 2Smad2 ProteinSmad3 ProteinTransforming Growth Factor betaTransforming Growth Factor beta1LysineSIRT2 protein, humanSirtuin 2Smad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanTransforming Growth Factor betaTransforming Growth Factor beta1

Identifiers

PMID37777567
PMCPMC10542381
OpenAlexW4387220055

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.