Evidence map›Paper›PMID 39169174›Full record

ArticleCell death and differentiation2024

Deficiency of thiosulfate sulfurtransferase mediates the dysfunction of renal tubular mitochondrial fatty acid oxidation in diabetic kidney disease.

Jia Xiu Zhang, Pei Pei Chen, Xue Qi Li, Liang Li, Qin Yi Wu, Gui Hua Wang, Xiong Zhong Ruan, Kun Ling Ma

Abstract read
In one paragraph

Article in Cell death and differentiation, 2024. 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
–field-weighted citation impact
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.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Regulated cell death: a multidimensional regulatory network in the pathogenesis of renal fibrosis.Apoptosis : an international journal on programmed cell death · 2026
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. HFrontiers in cell and developmental biology · 2026
    Review
  15. Review
  16. Article
  17. 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.

Jia Xiu ZhangInstitute of Nephrology, Zhong da Hospital, School of Medicine, Southeast University, Nanjing, China.ORCID 0000-0001-9238-2867
Pei Pei ChenInstitute of Nephrology, Zhong da Hospital, School of Medicine, Southeast University, Nanjing, China.
Xue Qi LiInstitute of Nephrology, Zhong da Hospital, School of Medicine, Southeast University, Nanjing, China.ORCID 0000-0002-8543-6887
Liang LiInstitute of Nephrology, Zhong da Hospital, School of Medicine, Southeast University, Nanjing, China.
Qin Yi WuInstitute of Nephrology, Zhong da Hospital, School of Medicine, Southeast University, Nanjing, China.
Gui Hua WangInstitute of Nephrology, Zhong da Hospital, School of Medicine, Southeast University, Nanjing, China.
Xiong Zhong RuanCentre for Lipid Research, Key Laboratory of Molecular Biology on Infectious Diseases, Ministry of Education, Chongqing Medical University, Chongqing, China.ORCID 0000-0001-5199-4971
Kun Ling MaInstitute of Nephrology, Zhong da Hospital, School of Medicine, Southeast University, Nanjing, China. klma@zju.edu.cn.

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82170736, 81970629, 82370716Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LHDMY23H070002
6 · The paper itself

Abstract

One of the main characteristics of diabetic kidney disease (DKD) is abnormal renal tubular fatty acid metabolism, especially defective fatty acid oxidation (FAO), accelerating tubular injury and tubulointerstitial fibrosis. Thiosulfate sulfurtransferase (TST), a mitochondrial enzyme essential for sulfur transfer, is reduced in metabolic diseases like diabetes and obesity. However, the potential role of TST in regulating fatty acid metabolic abnormalities in DKD remains unclear. Here, our data revealed decreased TST expression in the renal cortex of DKD patients. TST deficiency exacerbated tubular impairment in both diabetic and renal fibrosis mouse models, while sodium thiosulfate treatment or TST overexpression mitigated renal tubular injury with high-glucose exposure. TST downregulation mediated the decrease in S-sulfhydration of very long-chain specific acyl-CoA dehydrogenase, resulting in mitochondrial FAO dysfunction. This sequence of events exacerbates the progression of tubulointerstitial injury in DKD. Together, our findings demonstrate TST as a regulator of renal tubular injury in DKD.

Indexed as

Diabetic NephropathiesFatty AcidsKidney TubulesMitochondriaOxidation-ReductionThiosulfate SulfurtransferaseAnimalsFemaleHumansMaleMiceMice, Inbred C57BLFatty AcidsThiosulfate Sulfurtransferase

Identifiers

PMID39169174
PMCPMC11618416

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.