Evidence map›Paper›PMID 37539197›Full record

ArticleHeliyon2023

Proteomics reveals defective peroxisomal fatty acid oxidation during the progression of acute kidney injury and repair.

Jia Chen, Quan-You Zheng, Li-Ming Wang, Jia Luo, Ke-Hong Chen, Ya-Ni He

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.6field-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

14 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Selective autophagy in kidney health and disease.Nature reviews. Nephrology · 2026
    Review
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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 3 institutions in 1 country.

Jia ChenDepartment of Nephrology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Quan-You ZhengDepartment of Nephrology and Urology, The 958th Hospital, The First Affiliated Hospital, Army Medical University, Chongqing, 400020, China.
Li-Ming WangDepartment of Nephrology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Jia LuoDepartment of Nephrology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Ke-Hong ChenDepartment of Nephrology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Ya-Ni HeDepartment of Nephrology, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Army Medical University · CNChongqing Medical University · CNDaping Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) is characterized by a rapid decrease in renal function with high mortality and risk of progression to chronic kidney disease (CKD). Ischemia and reperfusion injury (IRI) is one of the major causes of AKI. However, the cellular and molecular responses of the kidney to IRI are complex and not fully understood. Herein, we conducted unbiased proteomics and bioinformatics analyses in an IRI mouse model on days 3, 7, and 21, and validated the results using IRI, unilateral ureteral obstruction (UUO), and biopsies from patients with AKI or CKD. The results indicated an obvious temporal expression profile of differentially expressed proteins and highlighted impaired lipid metabolism during the progression of AKI to CKD. Acyl-coenzyme A oxidase 1 (Acox1), the first rate-limiting enzyme of peroxisomal fatty acid beta-oxidation, was then selected, and its disturbed expression in the two murine models validated the proteomic findings. Accordingly, Acox1 expression was significantly downregulated in renal biopsies from patients with AKI or CKD, and its expression was negatively correlated with kidney injury score. Furthermore, in contrast to the decreased Acox1 expression, lipid droplet accumulation was remarkably increased in these renal tissues, suggesting dysregulation of fatty acid oxidation. In conclusion, our results suggest that defective peroxisomal fatty acid oxidation might be a common pathological feature in the transition from AKI to CKD, and that Acox1 is a promising intervention target for kidney injury and repair.

Indexed as

Acox1Acute kidney injuryFatty acid oxidationMaladaptive repairProteome

Identifiers

PMID37539197
PMCPMC10395357
OpenAlexW4384564990

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.