Evidence map›Paper›PMID 41266926›Full record

ArticleIn vitro cellular & developmental biology. Animal2026

M2 macrophages alleviate podocyte apoptosis induced by supernatant of glomerular mesangial cells with aIgA1 via targeting UCHL1.

Yuanjie Lin, Bingqing Liu, Zhengjie Wang, Lantao Dai

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Article in In vitro cellular & developmental biology. Animal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Yuanjie LinDepartment of Nephrology, The Affiliated Hospital of Putian University, Putian, 351100, Fujian, China.
Bingqing LiuDepartment of Nephrology, The Affiliated Hospital of Putian University, Putian, 351100, Fujian, China.
Zhengjie WangDepartment of Nephrology, The Affiliated Hospital of Putian University, Putian, 351100, Fujian, China.
Lantao DaiDepartment of Nephrology, The Affiliated Hospital of Putian University, Putian, 351100, Fujian, China. Dailantao1@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunoglobulin A (IgA) nephropathy (IgAN) is characterized by the deposition of IgA1 in the glomerular mesangium, which induces secondary glomerular and tubulointerstitial inflammation and subsequently leads to podocyte apoptosis and fibrosis. This condition often progresses to end-stage renal disease and lacks effective targeted treatment. Our study aimed to explore the role of M2 macrophage-mediated Ubiquitin C-terminal hydrolase L1 (UCHL1) expression in podocytes and its potential impact on the progression of IgAN. This study established an IgAN cellular model by exposing podocytes to aggregated IgA1 (aIgA1)-treated glomerular mesangial cells supernatants and assessed the impact of M2 macrophage polarization on UCHL1 expression and podocyte apoptosis. Additionally, we utilized siRNA technology and overexpression constructs to investigate the direct effects of UCHL1 modulation on podocyte apoptosis. The supernatant from aIgA1-treated glomerular mesangial cells significantly induced apoptosis in podocytes. Based on this, M2 macrophage polarization was induced using interleukin (IL)-4. The results showed that M2 macrophages (CD163

Indexed as

ApoptosisImmunoglobulin AMacrophagesMesangial CellsPodocytesUbiquitin ThiolesteraseAnimalsCytokinesGlomerulonephritis, IGAMiceCytokinesImmunoglobulin AUbiquitin ThiolesteraseUchl1 protein, mouseApoptosisImmunoglobulin A nephropathyM2 macrophagesPodocyteUCHL1

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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.