ArticleHuman genetics2024
Identification of TACSTD2 as novel therapeutic targets for cisplatin-induced acute kidney injury by multi-omics data integration.
Article in Human genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Icaritin Ameliorates Cisplatin-Induced Mitochondrial Metabolic Dysfunction-Associated Nephrotoxicity and Synergistically Potentiates Its Antitumor Efficacy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Involvement of HMGB1-mediated ferroptosis in systemic diseases.Frontiers in cell and developmental biology · 2025Review
- Multi-Omics Integration in Nephrology: Advances, Challenges, and Future Directions.Seminars in nephrology · 2024Review
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Cisplatin-induced acute kidney injury (CP-AKI) is a common complication in cancer patients. Although ferroptosis is believed to contribute to the progression of CP-AKI, its mechanisms remain incompletely understood. In this study, after initially processed individual omics datasets, we integrated multi-omics data to construct a ferroptosis network in the kidney, resulting in the identification of the key driver TACSTD2. In vitro and in vivo results showed that TACSTD2 was notably upregulated in cisplatin-treated kidneys and BUMPT cells. Overexpression of TACSTD2 accelerated ferroptosis, while its gene disruption decelerated ferroptosis, likely mediated by its potential downstream targets HMGB1, IRF6, and LCN2. Drug prediction and molecular docking were further used to propose that drugs targeting TACSTD2 may have therapeutic potential in CP-AKI, such as parthenolide, progesterone, premarin, estradiol and rosiglitazone. Our findings suggest a significant association between ferroptosis and the development of CP-AKI, with TACSTD2 playing a crucial role in modulating ferroptosis, which provides novel perspectives on the pathogenesis and treatment of CP-AKI.
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Registered trials
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