Evidence map›Paper›PMID 38584832›Full record

ArticleOpen medicine (Warsaw, Poland)2024

CD36-mediated podocyte lipotoxicity promotes foot process effacement.

Wei Hua, Lan Peng, Xue-Mei Chen, XuShun Jiang, JianGuo Hu, Xian-Hong Jiang, Xu Xiang, Jiangmin Wan, Yingfei Long, Jianqiong Xiong and 2 more

Abstract read
In one paragraph

Article in Open medicine (Warsaw, Poland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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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

12 authors.

Wei HuaDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical and Pharmaceutical College, Chongqing 400000, China.
Lan PengBasic Department, Chongqing Medical and Pharmaceutical College, Chongqing 401331, China.
Xue-Mei ChenEmergency Department, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400042, China.
XuShun JiangDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400042, China.
JianGuo HuDepartment of Obstetrics and Gynecology, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Xian-Hong JiangDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical and Pharmaceutical College, Chongqing 400000, China.
Xu XiangDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical and Pharmaceutical College, Chongqing 400000, China.
Jiangmin WanDepartment of Nephrology, People's Hospital of Qijiang District, Chongqing 401420, China.
Yingfei LongDepartment of Obstetrics and Gynecology, The Third Affiliated Hospital of Chongqing Medical University, Chongqing, 401120, China.
Jianqiong XiongHospital of Chongqing University, Chongqing, 400044, China.
Xueyi MaDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical and Pharmaceutical College, Chongqing 400000, China.
Xiaogang DuDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Youyi Road 1, Chongqing 400042, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Lipid metabolism disorders lead to lipotoxicity. The hyperlipidemia-induced early stage of renal injury mainly manifests as podocyte damage. CD36 mediates fatty acid uptake and the subsequent accumulation of toxic lipid metabolites, resulting in podocyte lipotoxicity. Methods: Male Sprague-Dawley rats were divided into two groups: the normal control group and the high-fat diet group (HFD). Podocytes were cultured and treated with palmitic acid (PA) and sulfo- Results: Podocyte foot process (FP) effacement and marked proteinuria occurred in the HFD group. CD36 protein expression was upregulated in the HFD group and in PA-treated podocytes. PA-treated podocytes showed increased fatty acid accumulation, reactive oxygen species (ROS) production, and actin cytoskeleton rearrangement. However, pretreatment with the CD36 inhibitor SSO decreased lipid accumulation and ROS production and alleviated actin cytoskeleton rearrangement in podocytes. The antioxidant N-acetylcysteine suppressed PA-induced podocyte FP effacement and ROS generation. Conclusions: CD36 participated in fatty acid-induced FP effacement in podocytes via oxidative stress, and CD36 inhibitors may be helpful for early treatment of kidney injury.

Indexed as

CD36foot process effacementpalmitic acidpodocyteROS

Identifiers

PMID38584832
PMCPMC10996993

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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.