ArticleRedox biology2018
Extracellular acidification induces ROS- and mPTP-mediated death in HEK293 cells.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 91 citations in OpenAlex.
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- Modulation of mitochondrial dysfunction: Mechanisms and strategies for the use of natural products to treat stroke.Neural regeneration research · 2026Article
- Yeast Phenomic Analysis Reveals DNA Repair, pH Homeostasis, and Ribosomal Biogenesis as Modulators of Anticancer Ruthenium Complex KP1019.International journal of molecular sciences · 2026Article
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- Endoplasmic Reticulum Stress: Triggers Microenvironmental Regulation and Drives Tumor Evolution.Cancer medicine · 2025Review
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- OMP38 of Carbapenem-Resistant Acinetobacter Baumannii-Mediated mtDNA Release Activates the cGAS-STING Signaling to Induce Inflammatory Response.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Inhibition of acid-sensing receptor GPR4 attenuates neuronal ferroptosis via RhoA/YAP signaling in a rat model of subarachnoid hemorrhage.Free radical biology & medicine · 2024Article
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- Construction of an ER stress-related prognostic signature for predicting prognosis and screening the effective anti-tumor drug in osteosarcoma.Journal of translational medicine · 2024Article
- Role of S100 and YKL40 on Intraventricular Cerebral Hemorrhages in the Preterm Infant and the Neuroprotective Role of miR-138- siRNAs-HIF-1a and miR-21-siRNAs-HVCN1 in Neonatal Mice with Nerve Injury.Current medicinal chemistry · 2024Article
- Benfotiamine protects MPTP-induced Parkinson's disease mouse model via activating Nrf2 signaling pathway.PloS one · 2024Article
- The Role of Epicardial Adipose Tissue-Derived Proteins in Heart Failure with Preserved Ejection Fraction and Atrial Fibrillation: A Bioinformatics Analysis.Journal of inflammation research · 2024Article
- Mitochondrial inorganic polyphosphate is required to maintain proteostasis within the organelle.Frontiers in cell and developmental biology · 2024Article
- Revisiting the Use of Normal Saline for Peritoneal Washing in Ovarian Cancer.International journal of molecular sciences · 2023Review
- The cGAS-STING pathway-dependent sensing of mitochondrial DNA mediates ocular surface inflammation.Signal transduction and targeted therapy · 2023Article
- Estrogen antagonizes ASIC1a-induced chondrocyte mitochondrial stress in rheumatoid arthritis.Journal of translational medicine · 2022Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The extracellular pH (pHe) is a key determinant of the cellular (micro)environment and needs to be maintained within strict boundaries to allow normal cell function. Here we used HEK293 cells to study the effects of pHe acidification (24h), induced by mitochondrial inhibitors (rotenone, antimycin A) and/or extracellular HCl addition. Lowering pHe from 7.2 to 5.8 reduced cell viability by 70% and was paralleled by a decrease in cytosolic pH (pHc), hyperpolarization of the mitochondrial membrane potential (Δψ), increased levels of hydroethidine-oxidizing ROS and stimulation of protein carbonylation. Co-treatment with the antioxidant α-tocopherol, the mitochondrial permeability transition pore (mPTP) desensitizer cyclosporin A and Necrostatin-1, a combined inhibitor of Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and Indoleamine 2,3-dioxygenase (IDO), prevented acidification-induced cell death. In contrast, the caspase inhibitor zVAD.fmk and the ferroptosis inhibitor Ferrostatin-1 were ineffective. We conclude that extracellular acidification induces necroptotic cell death in HEK293 cells and that the latter involves intracellular acidification, mitochondrial functional impairment, increased ROS levels, mPTP opening and protein carbonylation. These findings suggest that acidosis of the extracellular environment (as observed in mitochondrial disorders, ischemia, acute inflammation and cancer) can induce cell death via a ROS- and mPTP opening-mediated pathogenic mechanism.
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Registered trials
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