ArticleRenal failure2025
A multi-omics landscape of programmed cell death in acetaminophen-induced acute kidney injury.
Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- Disulfidptosis: Mechanisms, evidence boundaries, and translational opportunities.Redox biology · 2026Review
- pH-Responsive Carboxymethyl Cellulose-Encapsulating Hesperidin-Selenium Nanoparticles Attenuate Paracetamol-Induced Acute Kidney Injury via Keap-1/Nrf2, NF-κB, and Mitochondrial Apoptosis Modulation.International journal of molecular sciences · 2026Article
- Integrative multi-omics analysis identifies microbial dysbiosis and functional metabolic reprogramming in acute kidney injury.Frontiers in medicine · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acetaminophen (APAP) overdose is a known cause of acute kidney injury, yet the underlying molecular mechanisms remain incompletely understood. In this study, we conducted integrated transcriptomic, proteomic, and phosphoproteomic analyses of kidney tissues from mice with early-stage APAP-induced nephrotoxicity and corresponding controls. A total of 884 genes related to 13 distinct forms of programmed cell death (PCD)-including alkaliptosis, apoptosis, autophagy, cuproptosis, disulfidptosis, entotic cell death, ferroptosis, lysosome-dependent cell death, necroptosis, netotic cell death, oxeiptosis, parthanatos, and pyroptosis-were systematically evaluated. Gene set variation analysis was employed to assess the activity of these pathways in APAP-injured kidneys. Moreover, phosphokinase profiling and
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