ArticleJournal of translational medicine2023
TRPA1 promotes cisplatin-induced acute kidney injury via regulating the endoplasmic reticulum stress-mitochondrial damage.
Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 22 citations in OpenAlex.
- Role of mitochondria-associated ER membranes in lipid metabolism: implications for renal lipotoxicity.Bioscience reports · 2026Review
- Mitochondrial-endoplasmic reticulum interactions in lung diseases.Cell death & disease · 2026Review
- Mechanical ventilation activates PERK/eIF2α and NOD1 pathways that contribute to NF-κB-driven inflammation in VILI.Respiratory research · 2026Article
- Deubiquitinase USP35 regulates MDM4 degradation to promote endothelial ferroptosis and renal injury progression.Cell death discovery · 2026Article
- Direct coupling and protective activation of DRP1 by the DNA-PKcs inhibitor KU-57788 synergizes with ferroptosis in anaplastic thyroid cancer cells.Cell death & disease · 2026Article
- Gut microbiota-metabolite interactions in cisplatin-induced acute kidney injury in rats.BMC microbiology · 2026Article
- DDX11/SKP2 Inhibits Cisplatin Sensitivity in Liver Cancer Cells by Regulating DNA Damage Repair and ER Stress.Applied biochemistry and biotechnology · 2026Article
- Buspirone attenuates cyclophosphamide-induced renal dysfunction in association with alterations in miR-205/EGLN2, Nrf2, and PERK/ATF4/CHOP signaling.Frontiers in pharmacology · 2026Article
- Mitochondrial dysfunction in sepsis-associated acute kidney injury: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Cisplatin Induces Inflammation by Activating IL-6 via Suppressing rno-let-7g-5p and rno-let-7f-5p Expression in Intestinal Epithelial Cells.International journal of medical sciences · 2026Article
- Ferroptosis: A Double-Edged Sword in Cisplatin-Based Cancer Therapy and Acute Kidney Injury.Cancer management and research · 2026Review
- Roxadustat alleviates cisplatin-induced acute kidney injury by regulating fatty acid oxidation and mitochondrial function.Renal failure · 2025Article
- Hydrogen Sulfide Attenuates Cisplatin-Induced Acute Kidney Injury via Dual Inhibition of Apoptosis and Pyroptosis.Biomedicines · 2025Article
- [Elevated expressions of GRP78/CHOP in lupus nephritis: their diagnostic value and association with PERK/IRE1α pathway-mediated renal cell apoptosis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Targeting Endoplasmic Reticulum Stress by Natural and Chemical Compounds Ameliorates Cisplatin-Induced Nephrotoxicity: A Review.Biological trace element research · 2025Review
- Acetylation in renal physiology and pathophysiology.Frontiers in pharmacology · 2025Review
- Anthraquinones fromDrug design, development and therapy · 2025Review
- Research progress on endoplasmic reticulum homeostasis in acute kidney injury.Frontiers in pharmacology · 2025Review
- TRPA1 aggravates osteoclastogenesis and osteoporosis through activating endoplasmic reticulum stress mediated by SRXN1.Cell death & disease · 2024Article
- Artesunate-Nanoliposome-TPP, a Novel Drug Delivery System That Targets the Mitochondria, Attenuates Cisplatin-Induced Acute Kidney Injury by Suppressing Oxidative Stress and Inflammatory Effects.International journal of nanomedicine · 2024Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCisplatin is a widely used and effective chemotherapeutic agent against cancer. However, nephrotoxicity is one of the most common side effects of cisplatin, and it can proceed to acute kidney injury (AKI). Studies have reported that activation of transient receptor potential ankyrin-1 (TRPA1) mediates cisplatin-induced renal tubular cytotoxic injury. The aim of this study was to investigate the mechanism of TRPA1 in promoting cisplatin-induced AKI through modulation of the endoplasmic reticulum stress (ERS)-mitochondrial damage.
methodsA cisplatin-induced HK-2 cell model in vitro and mouse model in vivo were established. The mechanism of TRPA1 promotes AKI was elucidated by H&E staining, TUNEL staining, transmission electron microscope (TEM), immunofluorescence, CCK-8 viability assays, flow cytometry, Western blotting, JC-1 assay, and enzyme linked immunosorbent assay (ELISA).
resultIn vivo and in vitro, HC-030031 reduced cisplatin-induced Scr and BUN level elevations; improved cisplatin-induced renal tissue injury, apoptosis, and mitochondrial dysfunction; elevated the reduced ERS-associated proteins glucose-regulated protein 78 (GRP78), glucose-regulated protein 75 (GRP75), and C/EBP homologous protein (CHOP) levels induced by cisplatin; reduced the elevated optic atrophy 1 (OPA1), mito-fusion 1 (MFN1), and mito-fusion 2 (MFN2) protein levels, and elevated phospho-dynamin-related protein 1 (p-DRP1) and mitochondrial fission factor (MFF) protein levels. HC-030031 also reduced the mitochondria-associated endoplasmic reticulum membrane (MAM) structure. In addition, TRPA1 agonists also decreased cell proliferation, increased apoptosis, and triggered mitochondrial dysfunction and calcium overload in HK-2 cells via modulation of MAM. ERS inhibitors and GRP75 inhibitors reversed these changes caused by TRPA1 agonists.
conclusionOur findings suggest that TRPA1 enhances cisplatin-induced AKI via modulation of ERS and mitochondrial damage.
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