ArticleNature communications2023
Cisplatin toxicity is counteracted by the activation of the p38/ATF-7 signaling pathway in post-mitotic C. elegans.
Article in Nature communications, 2023. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- Aloesin mitigates cisplatin-induced nephrotoxicity by suppressing NF-κB-mediated oxidative stress and modulating Bax/Bcl-2/caspase pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Epigenomic Profiling Positions ATF7 as a Core Regulator of Colonic Inflammation.Journal of cellular and molecular medicine · 2025Article
- Shaker/Kv1 potassium channel SHK-1 protects against pathogen infection and oxidative stress in C. elegans.PLoS genetics · 2025Article
- Renogrit selectively protects against cisplatin-induced injury in human renal tubular cells and in Caenorhabditis elegans by harmonizing apoptosis and mitophagy.Scientific reports · 2024Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Cisplatin kills proliferating cells via DNA damage but also has profound effects on post-mitotic cells in tumors, kidneys, and neurons. However, the effects of cisplatin on post-mitotic cells are still poorly understood. Among model systems, C. elegans adults are unique in having completely post-mitotic somatic tissues. The p38 MAPK pathway controls ROS detoxification via SKN-1/NRF and immune responses via ATF-7/ATF2. Here, we show that p38 MAPK pathway mutants are sensitive to cisplatin, but while cisplatin exposure increases ROS levels, skn-1 mutants are resistant. Cisplatin exposure leads to phosphorylation of PMK-1/MAPK and ATF-7 and the IRE-1/TRF-1 signaling module functions upstream of the p38 MAPK pathway to activate signaling. We identify the response proteins whose increased abundance depends on IRE-1/p38 MAPK activity as well as cisplatin exposure. Four of these proteins are necessary for protection from cisplatin toxicity, which is characterized by necrotic death. We conclude that the p38 MAPK pathway-driven proteins are crucial for adult cisplatin resilience.
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