Authors
Heping Niu, Jiangwei Man, Ziyi Li, Xuezhen Ma, Zhendong Tian, Rongrong Deng, Shujun Shi, Xiaochun Zhou, Li Huang, Jianqin Wang
Published in
Drug and chemical toxicology. Pages 1-15. Jul 30, 2026. Epub Jul 30, 2026.
Abstract
Aristolochic acids (AAs) are a class of well-known nephrotoxic compounds; however, the molecular mechanisms underlying AA-induced kidney injury remain incompletely understood. This study aimed to identify potential molecular targets and explore the mechanisms involved in AA-induced kidney injury, with particular emphasis on prostaglandin-endoperoxide synthase 2 (PTGS2). An integrated computational and experimental approach was applied. Candidate targets associated with AA exposure and kidney injury were identified through database mining, followed by enrichment and network analyses to determine key regulatory genes. Molecular docking and molecular dynamics simulations were performed to evaluate AA-target interactions, and the association between PTGS2 and kidney injury was further assessed using two-sample Mendelian randomization based on genome-wide association study data. Experimental validation was conducted in an acute AAI-induced C57BL/6 mouse model through evaluation of renal function, histopathology, and PTGS2 expression. PTGS2 was identified as a central candidate gene associated with AA-induced kidney injury and exhibited stable binding with AA in silico. In vivo, AAI exposure caused renal dysfunction and histopathological alterations accompanied by reduced PTGS2 expression. These findings identified PTGS2 as a candidate molecular target involved in AA-induced kidney injury and provided a foundation for further mechanistic research.
PMID:
42529901
Bibliographic data and abstract were imported from PubMed on 30 Jul 2026.
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