Evidence map›Paper›PMID 36433732›Full record

ArticleCell proliferation2023

Sirt3 mitigates LPS-induced mitochondrial damage in renal tubular epithelial cells by deacetylating YME1L1.

Yonghong Jian, Yifei Yang, Lingli Cheng, Xueyan Yang, Hongyan Liu, Wei Li, Yuhan Wan, Dingping Yang

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. The Role of Sirt3 in Kidney Health and Disease.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. MitoQ alleviates mitochondria damage in sepsis-acute lung injury in a citrate synthase dependent manner.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review
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.

Yonghong JianDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China.ORCID https://orcid.org/0000-0002-9719-2103
Yifei YangDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China.
Lingli ChengDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China.
Xueyan YangDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China.
Hongyan LiuDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China.
Wei LiDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China.
Yuhan WanDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China.
Dingping YangDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China.
Wuhan University · CN

Funding

Dingping Yang 81670631
6 · The paper itself

Abstract

Acute kidney injury (AKI) is often secondary to sepsis. Increasing evidence suggests that mitochondrial dysfunction contributes to the pathological process of AKI. In this study, we aimed to examine the regulatory roles of Sirt3 in Lipopolysaccharide (LPS)-induced mitochondrial damage in renal tubular epithelial cells (TECs). Sirt3 knockout mice were intraperitoneally injected with LPS, and cultured TECs were stimulated with LPS to evaluate the effects of Sirt3 on mitochondrial structure and function in TECs. Electron microscopy was used to assess mitochondrial morphology. Immunofluorescence staining was performed to detect protein expression and examine mitochondrial morphology. Western blotting was used to quantify protein expression. We observed that LPS increased apoptosis, induced disturbances in mitochondrial function and dynamics, and downregulated Sirt3 expression in a sepsis-induced AKI mouse model and human proximal tubular (HK-2) cells in vitro. Sirt3 deficiency further exacerbated LPS-induced renal pathological damage, apoptosis and disturbances in mitochondrial function and dynamics. On the contrary, Sirt3 overexpression in HK-2 cells alleviated these lesions. Functional studies revealed that Sirt3 overexpression alleviated LPS-induced mitochondrial damage and apoptosis in TECs by promoting OPA1-mediated mitochondrial fusion through the deacetylation of i-AAA protease (YME1L1), an upstream regulatory molecule of OPA1. Our study has identified Sirt3 as a vital factor that protects against LPS-induced mitochondrial damage and apoptosis in TECs via the YME1L1-OPA1 signaling pathway.

Indexed as

Acute Kidney InjurySepsisSirtuin 3AnimalsApoptosisATPases Associated with Diverse Cellular ActivitiesEpithelial CellsHumansLipopolysaccharidesMetalloendopeptidasesMiceMice, KnockoutMitochondrial ProteinsATPases Associated with Diverse Cellular ActivitiesLipopolysaccharidesMetalloendopeptidasesMitochondrial ProteinsSIRT3 protein, humanSirt3 protein, mouseSirtuin 3YME1L1 protein, human

Identifiers

PMID36433732
PMCPMC9890524
OpenAlexW4310297346

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.