ArticleCell death & disease2021
Caspase 3/GSDME-dependent pyroptosis contributes to chemotherapy drug-induced nephrotoxicity.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 1 of them a synthesis that pooled it.
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Who cites it
133 citing papers in PubMed, 1 synthesis or guideline pooled it, 206 citations in OpenAlex.
- Biomarker selection and reporting architecture in human proximal tubularFrontiers in toxicology · 2026Pooled it
- Polydatin alleviates adenine-induced nephropathy in mice.Renal failure · 2026Article
- Fibrinogen-like protein 2-complement C3 interaction exacerbates tubular inflammation in acute kidney injury by elevating complement C3a levels.Renal failure · 2026Article
- Programmed cell death in inflammation: interactions and holistic perspective.Cellular & molecular immunology · 2026Review
- DeepSAT-guided discovery of sesquiterpenoid dimers from Inula japonica and identification of a natural pyroptosis inducer targeting the ROS-caspase-3-GSDME pathway.Archives of pharmacal research · 2026Article
- Hydroxytyrosol Restrains NLRP3 Inflammasome Activation and Pyroptosis Through the TLR4/NF-κB Pathway to Prevent Mycoplasma gallisepticum-Inflammation.Poultry science · 2026Article
- Pyroptosis as a novel therapeutic target in glioblastoma multiforme: Mechanisms, molecular insights, and therapeutic potential.Molecular therapy. Nucleic acids · 2026Review
- Zwitterionic Nanoplatform-Mediated Photopyroptosis for Abscopal Effect-Enhanced Cancer Immunotherapy.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Chlamydia psittaci induces GSDME-mediated pyroptosis via the ROS-JNK signaling pathway.Molecular and cellular biochemistry · 2026Article
- VALD-3 Induces GSDME-Dependent Pyroptosis via ROS/JNK/Bax Pathway in Triple-Negative Breast Cancer Cells.Biochemical genetics · 2026Article
- Review
- USP9X regulates copper-induced CASP9/CASP3/GSDME-dependent pyroptosis by deubiquitinating JAK1.Apoptosis : an international journal on programmed cell death · 2026Article
- Article
- MYBL2 impedes cisplatin sensitivity through suppressing GSDME-mediated pyroptosis in lung adenocarcinoma.Cell death discovery · 2026Article
- BIRC6 prevents GSDME-mediated pyroptosis and promotes cisplatin resistance via a non-canonical UBC domain-dependent steric hindrance.Cell communication and signaling : CCS · 2026Article
- Pyroptosis in endometritis: Molecular mechanisms, pathogenic roles, and therapeutic opportunities.iScience · 2026Review
- Tetrahydropalmatine may alleviate doxorubicin-induced renal injury by activating the Sirt3-mediated Nrf2/HO-1 pathway.Biology direct · 2026Article
- NEDD4L-mediated Gasdermin D and E ubiquitination regulates cell death and tissue injury.Cell death and differentiation · 2026Article
- Harnessing pyroptosis in breast cancer therapy: immunological mechanisms and emerging biomaterial strategies.Cell death discovery · 2026Review
- Corilagin induces pyroptosis in AML cells by activating the TXNIP-caspase-3-GSDME pathway.Annals of hematology · 2026Article
73 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemotherapy drug-induced nephrotoxicity limits clinical applications for treating cancers. Pyroptosis, a newly discovered programmed cell death, was recently reported to be associated with kidney diseases. However, the role of pyroptosis in chemotherapeutic drug-induced nephrotoxicity has not been fully clarified. Herein, we demonstrate that the chemotherapeutic drug cisplatin or doxorubicin, induces the cleavage of gasdermin E (GSDME) in cultured human renal tubular epithelial cells, in a time- and concentration-dependent manner. Morphologically, cisplatin- or doxorubicin-treated renal tubular epithelial cells exhibit large bubbles emerging from the cell membrane. Furthermore, activation of caspase 3, not caspase 9, is associated with GSDME cleavage in cisplatin- or doxorubicin-treated renal tubular epithelial cells. Meanwhile, silencing GSDME alleviates cisplatin- or doxorubicin-induced HK-2 cell pyroptosis by increasing cell viability and decreasing LDH release. In addition, treatment with Ac-DMLD-CMK, a polypeptide targeting mouse caspase 3-Gsdme signaling, inhibits caspase 3 and Gsdme activation, alleviates the deterioration of kidney function, attenuates renal tubular epithelial cell injury, and reduces inflammatory cytokine secretion in vivo. Specifically, GSDME cleavage depends on ERK and JNK signaling. NAC, a reactive oxygen species (ROS) inhibitor, reduces GSDME cleavage through JNK signaling in human renal tubular epithelial cells. Thus, we speculate that renal tubular epithelial cell pyroptosis induced by chemotherapy drugs is mediated by ROS-JNK-caspase 3-GSDME signaling, implying that therapies targeting GSDME may prove efficacious in overcoming chemotherapeutic drug-induced nephrotoxicity.
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Registered trials
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.