Evidence map›Paper›PMID 42560283›Full record

ArticleMediators of inflammation2026

Tissue Expression of NLRP3, IL-1β, and IL-18 in Glomerular and Interstitial Inflammation Associated With Diabetic Nephropathy.

Bruna de Freitas Oliveira, Liliane Silvano Araújo, Crislaine Aparecida da Silva, Laura Penna Rocha, Raíssa Bernardes da Silva, Marlene Antônia Dos Reis, Rafael Obata Trevisan, Bruna Cunha Zaidan, Juliana Reis Machado

Abstract read
In one paragraph

Article in Mediators of inflammation, 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. Article
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

9 authors.

Bruna de Freitas OliveiraKidney Research Center, Department of Pathology, Genetics and Evolution, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil, uftm.edu.br.ORCID https://orcid.org/0009-0000-6085-5965
Liliane Silvano AraújoKidney Research Center, Department of Pathology, Genetics and Evolution, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil, uftm.edu.br.ORCID https://orcid.org/0000-0002-0762-4014
Crislaine Aparecida da SilvaKidney Research Center, Department of Pathology, Genetics and Evolution, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil, uftm.edu.br.ORCID https://orcid.org/0000-0002-0615-1446
Laura Penna RochaKidney Research Center, Department of Pathology, Genetics and Evolution, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil, uftm.edu.br.ORCID https://orcid.org/0000-0001-6554-0241
Raíssa Bernardes da SilvaKidney Research Center, Department of Pathology, Genetics and Evolution, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil, uftm.edu.br.ORCID https://orcid.org/0000-0002-2802-3808
Marlene Antônia Dos ReisKidney Research Center, Department of Pathology, Genetics and Evolution, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil, uftm.edu.br.ORCID https://orcid.org/0000-0003-2523-2097
Rafael Obata TrevisanKidney Research Center, Department of Pathology, Genetics and Evolution, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil, uftm.edu.br.ORCID https://orcid.org/0000-0002-4509-9142
Bruna Cunha ZaidanKidney Research Center, Department of Pathology, Genetics and Evolution, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil, uftm.edu.br.ORCID https://orcid.org/0000-0001-7926-5199
Juliana Reis MachadoKidney Research Center, Department of Pathology, Genetics and Evolution, Institute of Biological and Natural Sciences, Federal University of Triângulo Mineiro, Uberaba, Minas Gerais, Brazil, uftm.edu.br.ORCID https://orcid.org/0000-0002-8673-7788

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico 313894/2023-0Fundação de Amparo à Pesquisa do Estado de Minas Gerais APQ-02831-23
6 · The paper itself

Abstract

Activation of the NLRP3 inflammasome and its downstream cytokines IL-1β and IL-18 has been increasingly associated with the inflammatory mechanisms underlying diabetic nephropathy (DN), the leading cause of chronic kidney disease and end-stage renal disease worldwide. This study investigated the expression of these inflammatory mediators in renal tissue from patients with DN. Eighty renal biopsies from adult patients (≥18 years) with a histopathological diagnosis of DN and 22 control samples obtained from autopsies were analyzed. NLRP3, IL-1β, and IL-18 expression was assessed by immunohistochemistry, and semi-quantitative analysis was performed to determine the proportion of immunostained cells in the glomerular and interstitial compartments. A significant increase in immunostaining for all three mediators was observed in mesangial cells, podocytes, endothelial cells, and the interstitium of DN samples compared with controls (p < 0.05). Positive and significant correlations were found between NLRP3 and IL-1β in endothelial cells (p < 0.0001; rS = 0.4720) and in the interstitium (p = 0.0230; rS = 0.2540), as well as between NLRP3 and IL-18 in podocytes (p = 0.0055; rS = 0.3074). Moreover, interstitial expression of NLRP3 and IL-1β correlated positively with serum creatinine levels (p = 0.0015; rS = 0.3708; and p = 0.0029; rS = 0.3480, respectively), suggesting an association between inflammasome-mediated inflammation and renal dysfunction. Collectively, these findings indicate that the NLRP3/IL-1β/IL-18 axis plays a central role in glomerular and interstitial injury in DN, supporting its potential as a prognostic biomarker and a promising therapeutic target for disease modulation.

Indexed as

Diabetic NephropathiesInflammationInterleukin-18Interleukin-1betaKidney GlomerulusNLR Family, Pyrin Domain-Containing 3 ProteinAdultAgedFemaleHumansImmunohistochemistryInflammasomesMaleMiddle AgedPodocytesIL18 protein, humanInflammasomesInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humandiabetic nephropathyinterleukin-18interleukin-1βNLRP3 inflammasomerenal inflammation

Identifiers

PMID42560283
PMCPMC13446144

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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.