Evidence map›Paper›PMID 41574094›Full record

ArticleKidney diseases (Basel, Switzerland)

UCP2-Driven Fatty Acid Oxidation Promotes Macrophage M2 Polarization and Renal Fibrosis.

Xingyue Wang, Yuxi Li, Liu Li, Xinyan Gu, Chunsun Dai, Lei Jiang

Abstract read
In one paragraph

Article in Kidney diseases (Basel, Switzerland). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Xingyue WangCenter for Kidney Diseases, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yuxi LiCenter for Kidney Diseases, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Liu LiCenter for Kidney Diseases, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Xinyan GuCenter for Kidney Diseases, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Chunsun DaiCenter for Kidney Diseases, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Lei JiangCenter for Kidney Diseases, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: During renal fibrosis, macrophages play a crucial role in multiple processes, such as initiating inflammation, mediating tissue repair, and promoting interstitial fibrosis. Macrophage polarization is a key determinant of their functional properties. This study aimed to investigate the roles and mechanism of macrophages with distinct phenotype in renal fibrosis. Methods: We established unilateral ureteral obstruction and ischemia-reperfusion injury models using macrophage-specific Results: We indicated that the energy metabolism pattern is a key factor during macrophage phenotypic switching. Specifically, uncoupling protein 2 (UCP2), a mitochondrial inner membrane protein, was found to regulate the metabolic profile of macrophages. Knockout of Conclusion: In summary, we identified UCP2 as a key regulator of macrophage metabolic reprogramming and a critical promoter of renal fibrosis, suggesting that targeting UCP2 represents a promising therapeutic strategy.

Indexed as

Fatty acid oxidationMacrophageMetabolic reprogrammingRenal interstitial fibrosisUCP2

Identifiers

PMID41574094
PMCPMC12820707

What OpenQuestion holds

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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.