Evidence map›Paper›PMID 39744137›Full record

ArticleFrontiers in pharmacology2024

PM2.5-induced oxidative stress upregulates PLA2R expression in the lung and is involved in the pathogenesis of membranous nephropathy through extracellular vesicles.

Wang Zhang, Jiating Chen, Ye Yuan, Jiao Luo, Zhanmei Zhou, Guobao Wang

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Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

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0cells of the map it votes in
12citing papers in PubMed
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1 · What the graph read from it

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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

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3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. Article
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  6. Chronic PMScientific reports · 2026
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4 · The record

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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.

Wang Zhang *Renal Division, State Key Laboratory of Organ Failure Research, National Clinical Research Center for Kidney Disease, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jiating Chen *Department of Nephrology, The Second Affiliated Hospital of Shenzhen University, Shenzhen, China.
Ye YuanRenal Division, State Key Laboratory of Organ Failure Research, National Clinical Research Center for Kidney Disease, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jiao LuoRenal Division, State Key Laboratory of Organ Failure Research, National Clinical Research Center for Kidney Disease, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zhanmei ZhouRenal Division, State Key Laboratory of Organ Failure Research, National Clinical Research Center for Kidney Disease, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Guobao WangRenal Division, State Key Laboratory of Organ Failure Research, National Clinical Research Center for Kidney Disease, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Particulate matter (PM2.5) has been implicated in the development of membranous nephropathy (MN), but the underlying mechanism has yet to be fully understood. Oxidative stress is an essential factor of PM2.5-related toxicity and plays a significant role in the exposure of target antigenic epitopes in MN. This study aims to explore the pathogenic effects of PM2.5 in facilitating the crosstalk between the lung and kidney in MN. Method: We examined oxidative stress indicators and the circulating levels of extracellular vesicles (EVs) in patients diagnosed with MN. Additionally, we assessed the expression of M-type phospholipase A2 receptor (PLA2R) in human lung tissue Results: We found that elevated serum markers of oxidative stress and increased levels of PLA2R + EVs correlated positively with anti-PLA2R antibody levels in the serum of patients with idiopathic MN (IMN). Notably, PLA2R expression was significantly higher in the lung tissue of smokers, suggesting a possible link between PLA2R and oxidative stress. Conclusion: Our study contributes new knowledge to the understanding of how environmental pollutants, such as PM2.5, cause kidney damage through oxidative stress and EV-mediated signaling. The findings pave the way for further research into therapeutic strategies targeting oxidative stress and EVs, which could potentially improve patient outcomes of MN, particularly in high-risk populations like smokers and those exposed to air pollution.

Indexed as

extracellular vesiclesmembranous nephropathyoxidative stressPLA2RPM 2.5

Identifiers

PMID39744137
PMCPMC11688400

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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.