Evidence map›Paper›PMID 35842903›Full record

ArticleCell proliferation2022

Sirt6 deficiency contributes to mitochondrial fission and oxidative damage in podocytes via ROCK1-Drp1 signalling pathway.

Zhaowei Chen, Wei Liang, Jijia Hu, Zijing Zhu, Jun Feng, Yiqiong Ma, Qian Yang, Guohua Ding

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Podocyte Metabolic Reprogramming and Targeted Therapy.Journal of the American Society of Nephrology : JASN · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Sirtuins in kidney health and disease.Nature reviews. Nephrology · 2024
    Review
  18. 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

8 authors at 1 institution in 1 country.

Zhaowei ChenDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.ORCID https://orcid.org/0000-0001-7165-4325
Wei LiangDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Jijia HuDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.ORCID https://orcid.org/0000-0002-8847-845X
Zijing ZhuDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Jun FengDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Yiqiong MaDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Qian YangDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Guohua DingDivision of Nephrology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.
Wuhan University · CN

Funding

Fundamental Research Funds for the Central Universities 2042021kf0120National Natural Science Foundation of China 81770687National Natural Science Foundation of China 82070713
6 · The paper itself

Abstract

objectivesIncreasing evidence suggests that mitochondrial dysfunction is the key driver of angiotensin II (Ang II)-induced kidney injury. This study was designed to investigate whether Sirtuin 6 (Sirt6) could affect Ang II-induced mitochondrial damage and the potential mechanisms. MATERIALS AND

methodsPodocyte-specific Sirt6 knockout mice were infused with Ang II and cultured podocytes were stimulated with Ang II to evaluate the effects of Sirt6 on mitochondrial structure and function in podocytes. Immunofluorescence staining was used to detect protein expression and mitochondrial morphology in vitro. Electron microscopy was used to assess mitochondrial morphology in mice. Western blotting was used to quantify protein expression.

resultsMitochondrial fission and decreased Sirt6 expression were observed in podocytes from Ang II-infused mice. In Sirt6-deficient mice, Ang II infusion induced increased apoptosis and mitochondrial fragmentation in podocytes than that in Ang II-infused wild-type mice. In cultured human podocytes, Sirt6 knockdown exacerbated Ang II-induced mitochondrial fission, whereas Sirt6 overexpression ameliorated the Ang II-induced changes in the balance between mitochondrial fusion and fission. Functional studies revealed that Sirt6 deficiency exacerbated mitochondrial fission by promoting dynamin-related protein 1 (Drp1) phosphorylation. Furthermore, Sirt6 mediated Drp1 phosphorylation by promoting Rho-associated coiled coil-containing protein kinase 1 (ROCK1) expression.

conclusionOur study has identified Sirt6 as a vital factor that protects against Ang II-induced mitochondrial fission and apoptosis in podocytes via the ROCK1-Drp1 signalling pathway.

Indexed as

PodocytesSirtuinsAngiotensin IIAnimalsApoptosisDynaminsHumansMiceMitochondrial DynamicsOxidative Stressrho-Associated KinasesAngiotensin IIDynaminsrho-Associated KinasesROCK1 protein, humanSIRT6 protein, humanSirt6 protein, mouseSirtuins

Identifiers

PMID35842903
PMCPMC9528772
OpenAlexW4285676998

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.