Evidence map›Paper›PMID 31678001›Full record

ArticleEBioMedicine2019

Uncoupling protein 1 inhibits mitochondrial reactive oxygen species generation and alleviates acute kidney injury.

Ping Jia, Xiaoli Wu, Tianyi Pan, Sujuan Xu, Jiachang Hu, Xiaoqiang Ding

Abstract read
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing 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

50 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Deciphering Uncoupling Proteins in Cellular Homeostasis and Metabolic Health.International journal of biological sciences · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. No UCP1 in the kidney.Molecular metabolism · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

6 authors.

Ping JiaDivision of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Kidney and Blood Purification Laboratory of Shanghai, Shanghai, China.
Xiaoli WuTraditional Chinese Medicine Pharmacology Laboratory, Longhua Hospital, Shanghai University of Tranditional Chinese Medicine, Shanghai, China.
Tianyi PanDivision of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Sujuan XuDivision of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Jiachang HuDivision of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.
Xiaoqiang DingDivision of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Medical Center of Kidney, Shanghai, China; Kidney and Dialysis Institute of Shanghai, Shanghai, China; Kidney and Blood Purification Laboratory of Shanghai, Shanghai, China; Hemodialysis quality control center of Shanghai, Shanghai, China. Electronic address: ding.xiaoqiang@zs-hospital.sh.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUncoupling protein 1 (UCP1) is predominantly found in brown adipose tissue mitochondria, and mediates energy dissipation to generate heat rather than ATP via functional mitochondrial uncoupling. However, little is known about its expression and function in kidney.

methodsWe carried out a mRNA microarray analysis in mice kidneys with ischemia reperfusion (IR) injury. The most dramatically downregulated gene UCP1 after IR was identified, and its role in generation of mitochondrial reactive oxygen species (ROS) and oxidative stress injury was assessed both in vitro and in vivo. Genetic deletion of UCP1 was used to investigate the effects of UCP1 on ischemia or cisplatin-indued acute kidney injury (AKI) in mice.

findingsUCP1 was located in renal tubular epithelial cells in kidney and downregulated in a time-dependent manner during renal IR. Deletion of UCP1 increased oxidative stress in kidneys and aggravated ischemia or cisplatin induced AKI in mice.Viral-based overexpression of UCP1 reduced mitochondrial ROS generation and apoptosis in hypoxia-treated tubular epithelial cells. Furthermore, UCP1 expression was regulated by peroxisome proliferator-activator receptor (PPAR) γ in kidneys during renal IR. Overexpression of PPAR-γ resembled UCP1-overexpression phenotype in vitro. Treatment with PPAR-γ agonist could induce UCP1 upregulation and provide protective effect against renal IR injury in UCP1

interpretationUCP1 protects against AKI likely by suppressing oxidative stress, and activation of UCP1 represents a potential therapeutic strategy for AKI. FUND: National Natural Science Foundation of China grants, Science and Technology Commission of Shanghai.

Indexed as

Acute Kidney InjuryAnimalsApoptosisDown-RegulationEpithelial CellsGene DeletionHumansKidneyKidney TubulesMaleMice, Inbred C57BLMitochondriaOxidative StressPPAR gammaReactive Oxygen SpeciesReperfusion InjuryPPAR gammaReactive Oxygen SpeciesUncoupling Protein 1Acute kidney injuryPeroxisome proliferator-activator receptor γReactive oxygen speciesUncoupling protein 1

Identifiers

PMID31678001
PMCPMC6945195

What OpenQuestion holds

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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.