Ogg1 regulates TGF‑β-Smad3 signalling and fibrosis progression in chronic kidney disease.

Ying Wang, Yan Liu, Bo Peng, Chan Zou, Guoping Yang, Jiefu Zhu, Hao Zhang, Jing Huang

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Article in Communications biology, 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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5 · Who and what money

Authors and funding

8 authors.

Ying WangDepartment of Nephrology, The Third Xiangya Hospital at Central South University, Changsha, China.

Yan LiuDepartment of Nephrology, The Third Xiangya Hospital at Central South University, Changsha, China.

Bo PengTransplantation Center, The Third Xiangya Hospital, Central South University, Changsha, China.

Chan ZouCenter for Clinical Pharmacology, the Third Xiangya Hospital, Central South University, Changsha, China.

Guoping YangCenter for Clinical Pharmacology, the Third Xiangya Hospital, Central South University, Changsha, China.

Jiefu ZhuDepartment of Organ Transplantation, Renmin Hospital of Wuhan University, Wuhan, China. jiefuzhu@whu.edu.cn.ORCID http://orcid.org/0000-0001-9105-022X

Hao ZhangDepartment of Nephrology, The Third Xiangya Hospital at Central South University, Changsha, China. zhanghaoliaoqing@163.com.ORCID http://orcid.org/0000-0002-2049-3485

Jing HuangDepartment of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China. rm001869@whu.edu.cn.ORCID http://orcid.org/0000-0002-7754-6023

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kidney fibrosis is a hallmark of chronic kidney disease (CKD) and a major contributor to progression toward end-stage renal disease. Here, we identify 8-oxoguanine DNA glycosylase 1 (Ogg1), a DNA repair enzyme, as a regulator of kidney fibrosis. Ogg1 expression is upregulated in experimental fibrosis models in male mice, including unilateral ureteral obstruction (UUO) and aristolochic acid (AA) nephropathy, as well as in kidney tissues from CKD patients. Genetic deletion of Ogg1 reduces fibrosis, tubular atrophy and fibrotic marker expression, and improves renal function in AA nephropathy. Mechanistically, Ogg1 interacts with phosphorylated Smad3 in the nucleus and promotes transcriptional regulation of profibrotic genes. Pharmacological inhibition of Ogg1 with TH5487 alleviates fibrosis in both UUO and AA nephropathy models, supporting Ogg1 as a potential therapeutic target in CKD.

Indexed as

DNA GlycosylasesRenal Insufficiency, ChronicSignal TransductionSmad3 ProteinTransforming Growth Factor betaAnimalsAristolochic AcidsDisease ProgressionFibrosisHumansKidneyMaleMiceMice, Inbred C57BLMice, KnockoutUreteral Obstructionaristolochic acid IAristolochic AcidsDNA GlycosylasesOgg1 protein, mouseoxoguanine glycosylase 1, humanSmad3 ProteinSmad3 protein, mouseTransforming Growth Factor beta

Identifiers

PMID42115320

DOI10.1038/s42003-026-10177-0

PMCPMC13470380

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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.