Evidence map›Paper›PMID 42464422›Full record

ArticleNephrology (Carlton, Vic.)2026

CORO1A, A Novel Upregulated Protein in Renal Tubular Epithelial Cells of Diabetic Nephropathy, Participates in Regulating Vesicular Trafficking and the Ferroptosis Pathway.

Shenghao Meng, Xitong Xu, Hongru Chen, Zhigang Zhang, Huijuan Wu, Chenyang Qi

Abstract read
In one paragraph

Article in Nephrology (Carlton, Vic.), 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

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Shenghao MengDepartment of Pathology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
Xitong XuDepartment of Pathology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
Hongru ChenDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Zhigang ZhangDepartment of Pathology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0001-7895-9332
Huijuan WuDepartment of Pathology, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0003-4681-4440
Chenyang QiDepartment of Nephrology, Institute of Nephrology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0002-0407-1346

Funding

National Natural Science Foundation of China 82100757ZHENGYl Scholar Scientific Research Project of Fudan University School of Basic Medical Sciences
6 · The paper itself

Abstract

aimDiabetic nephropathy (DN) is characterised by progressive renal tubular epithelial cell injury, yet underlying molecular mechanisms remain incompletely understood.

methodsDifferentially expressed genes (DEGs) in DN were identified through integrated GEO dataset analysis (GSE30529 and GSE175759). Protein-protein interaction networks identified hub genes. GO and KEGG enrichment analyses determined molecular mechanisms. Nephroseq v5 explored correlations between hub genes and clinical features. CORO1A expression was validated by immunohistochemistry and western blot in DN patients, diabetic db/db mice and high glucose-exposed HK-2 cells. Vps34 inhibition and CORO1A knockdown explored regulatory mechanisms in vesicular trafficking and ferroptosis.

resultsBioinformatics identified CORO1A as a phagosome-related core gene significantly upregulated in DN renal tubulointerstitium and correlated with eGFR, proteinuria, serum creatinine, blood pressure and age. External validation and experiments confirmed CORO1A upregulation in DN patients, diabetic mice and high glucose-exposed cells. Vps34 inhibition impaired lysosomal degradation flux and increased tubular injury markers, ferroptosis, ferritinophagy and CORO1A expression. CORO1A knockdown attenuated ferroptosis and lipid peroxidation, while rescue experiments with Ferrostatin-1 and Erastin confirmed the functional link between CORO1A, vesicular trafficking and ferroptosis.

conclusionCORO1A is elevated in diabetic renal tubular epithelial cells and regulates vesicular trafficking and ferroptosis. This mechanistic axis suggests CORO1A as a potential therapeutic target for mitigating tubular injury and diabetic nephropathy progression.

Indexed as

Diabetic NephropathiesEpithelial CellsFerroptosisKidney TubulesAnimalsCell LineHumansMaleMiceSignal TransductionUp-Regulationdiabetic nephropathyferritinophagyferroptosisrenal tubular epithelial cellvesicular trafficking

Identifiers

PMID42464422
PMCPMC13376232

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