Evidence map›Paper›PMID 42462511›Full record

ArticleClinics (Sao Paulo, Brazil)2026

LncRNA GATA3-AS1-mediated miR-2116-5p interaction modulates TCF12 and contributes to podocyte dysfunction in childhood nephrotic syndrome.

Xin Tong, Yong Zhao, Peng Huang

Abstract read
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Article in Clinics (Sao Paulo, Brazil), 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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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Xin TongDepartment of Nephrology, Dazhou Central Hospital, Dazhou, China.
Yong ZhaoJiangxi Beizheng Stell Cell Biotechnology Co., Ltd, Jiangxi, China.
Peng HuangDepartment of Nephrology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China; Key Laboratory of Medical Research Basic Guarantee for Immune-Related Diseases Research of Guangxi, Baise, China. Electronic address: huangpengdr@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesChildhood Nephrotic Syndrome (NS) is a common kidney disease. This study investigates the role of LncRNA GATA3-AS1 and miR-2116-5p in childhood NS and their impact on podocyte function.

methodsThis study employed qRT-PCR to detect the levels of GATA3-AS1 and miR-2116-5p in serum and evaluated their diagnostic value. An in vitro injury model was established by treating MPC5 podocytes with TGF-β1. Following the overexpression of GATA3-AS1, miR-2116-5p, or TCF12, cell proliferation, inflammatory responses, and oxidative stress were assessed. RNA interactions were examined using dual-luciferase reporter and RIP assays, and podocyte-specific proteins were analyzed by Western Blot.

resultsIn childhood NS patients, serum GATA3-AS1 is downregulated and miR-2116-5p upregulated, with a negative correlation. ROC curves show they have good diagnostic value. In vitro, GATA3-AS1 overexpression restored TGF-β1 -inhibited cell proliferation, reduced inflammatory factors, lowered MDA, and raised SOD activity, with miR-2116-5p mimic reversing this effect. Bioinformatics analysis revealed TCF12 as a high-confidence target gene of miR-2116-5p, and luciferase assays confirmed the binding between miR-2116-5p and TCF12. Childhood NS patients have lower serum TCF12 than controls, and TCF12 overexpression can repair miR-2116-5p -induced podocyte damage. TCF12 overexpression can restore the expression of podocyte marker proteins such as Synaptopodin and Podocin, and inhibit Cleaved Caspase-3-mediated apoptosis.

conclusionsLncRNA GATA3-AS1 is downregulated in pediatric NS and mediates the expression of miR-2116-5p, thereby influencing TCF12, a mechanism that may potentially have a protective effect on the kidneys in children.

Indexed as

Childhood nephrotic syndromeLncRNA GATA3-AS1miR-2116-–5pPodocyteTCF12

Identifiers

PMID42462511
PMCPMC13383947

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