Evidence map›Paper›PMID 41752063›Full record

ArticleInternational journal of molecular sciences2026

Extracellular Vesicles Facilitate the Crosstalk Between High Glucose-Stimulated Mesangial Cells and Healthy Podocytes to Mediate Injury Responses.

Antonio S Novaes, Raphael J F Felizardo, Niels O S Camara, Shipra Agrawal, Mirian A Boim

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

5 authors.

Antonio S NovaesDepartment of Medicine, Renal Division, Federal University of São Paulo, São Paulo 04024-002, Brazil.ORCID 0000-0002-8418-2504
Raphael J F FelizardoDepartment of Medicine, Renal Division, Federal University of São Paulo, São Paulo 04024-002, Brazil.ORCID 0000-0001-9650-6273
Niels O S CamaraDepartment of Medicine, Renal Division, Federal University of São Paulo, São Paulo 04024-002, Brazil.ORCID 0000-0001-5436-1248
Shipra AgrawalDepartment of Medicine, Division of Nephrology and Hypertension, Renaissance School of Medicine, Stony Brook University, Stony Brook, NY 11794, USA.ORCID 0000-0002-1111-9168
Mirian A BoimDepartment of Medicine, Renal Division, Federal University of São Paulo, São Paulo 04024-002, Brazil.ORCID 0000-0001-7500-8371

Funding

Mechanisms and Selective Modulation of PPARy for the Treatment of PodocytopathiesR01DK133440 · NIDDK · STATE UNIVERSITY NEW YORK STONY BROOK · PI AGRAWAL, SHIPRA · 2023 to 2025
$728k
Fundação de Amparo à Pesquisa do Estado de São Paulo 2015/23345-9Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP). 2017/00250-8NIDDK NIH HHS R01 DK133440
6 · The paper itself

Abstract

Mesangial cells (MCs) communicate with podocytes and contribute to podocyte damage in diabetes. We hypothesized that intercellular communication plays a critical role in glomerular injury in diabetic nephropathy (DN). This study investigated the role of extracellular vesicles (EVs) secreted by high glucose-treated MCs in podocyte dysfunction. MCs were cultured with normal or high glucose for 24 h, and control EVs (C-EVs) and high-glucose EVs (HG-EVs) were isolated and incubated with healthy podocytes. Immunofluorescence, qRT-PCR, and Western blotting assessed podocyte and profibrotic marker expression. High glucose increased the overall amount of EVs released by MCs, but not their size. HG-EVs induced upregulation of epithelial-mesenchymal transition (EMT) markers, including desmin and TGF-β1, and downregulation of podocyte markers alpha-actinin-4, synaptopodin, and P-cadherin. In a co-culture of high-glucose MCs and podocytes, an exosome secretion inhibitor attenuated these injurious effects. These data suggest that HG-EVs impair podocyte function and mediate communication between MCs and podocytes. Mesangial cell-derived EVs may represent potential therapeutic targets in DN.

Indexed as

Cell CommunicationExtracellular VesiclesGlucoseMesangial CellsPodocytesActininAnimalsCadherinsCells, CulturedCoculture TechniquesDesminDiabetic NephropathiesEpithelial-Mesenchymal TransitionHumansMiceMicrofilament ProteinsActininCadherinsDesminGlucoseMicrofilament ProteinsTransforming Growth Factor beta1diabetic nephropathyextracellular vesicleshigh-glucose conditionsintercellular communicationmesangial cellspodocyte damage

Identifiers

PMID41752063
PMCPMC12940433

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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.