ArticleFree radical biology & medicine2010
SOD1 and MitoTEMPO partially prevent mitochondrial permeability transition pore opening, necrosis, and mitochondrial apoptosis after ATP depletion recovery.
Article in Free radical biology & medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 141 citations in OpenAlex.
- Pseudomonas aeruginosa 3-oxo-C12HSL-induced apoptosis involves bitter taste receptor T2R14 and the mitochondrial calcium uniporter.Cell calcium · 2026Article
- Qualitative and flow cytometric evaluations of goat's frozen semen in Mito-TEMPO supplemented plant-based extender.BMC veterinary research · 2026Article
- Glucocorticoids regulate small extracellular vesicle (sEV) release via activation of nSMase2.bioRxiv : the preprint server for biology · 2025Article
- Optimizing Cryopreservation: The Effect of MitoTEMPO and Glycerol Ratios on Ram Semen Quality After Freezing and Thawing.Veterinary medicine and science · 2025Article
- Inhibition of VDAC1 oligomerization blocks cysteine deprivation-induced ferroptosis via mitochondrial ROS suppression.Cell death & disease · 2024Article
- Enhancing of Rabbit Sperm Cryopreservation with Antioxidants Mito-Tempo and Berberine.Antioxidants (Basel, Switzerland) · 2024Article
- From 2D to 3D In Vitro World: Sonodynamically-Induced Prooxidant Proapoptotic Effects of CCancers · 2024Article
- Effect of Sodium Thiosulfate Pre-Treatment on Renal Ischemia-Reperfusion Injury in Kidney Transplantation.International journal of molecular sciences · 2024Article
- DNA of neutrophil extracellular traps promote NF-κB-dependent autoimmunity via cGAS/TLR9 in chronic obstructive pulmonary disease.Signal transduction and targeted therapy · 2024Article
- Article
- Supplementation with MitoTEMPO before cryopreservation improves sperm quality and fertility potential of Piedmontese beef bull semen.Frontiers in veterinary science · 2024Article
- Sex-specific colonic mitochondrial dysfunction in the indomethacin-induced rat model of inflammatory bowel disease.Frontiers in physiology · 2024Article
- Reactive oxygen species drive foraging decisions in Caenorhabditis elegans.Redox biology · 2023Article
- Article
- Chronic oxidative stress adaptation in head and neck cancer cells generates slow-cyclers with decreased tumour growth in vivo.British journal of cancer · 2023Article
- Ethanolic Extract ofMetabolites · 2023Article
- Mitochondrial quality control in health and cardiovascular diseases.Frontiers in cell and developmental biology · 2023Review
- The dynamic interplay between cardiac mitochondrial health and myocardial structural remodeling in metabolic heart disease, aging, and heart failure.The journal of cardiovascular aging · 2023Article
- Protective roles of cytoplasmic p21Cell proliferation · 2022Article
- Contributions and Limitations of Mitochondria-Targeted and Non-Targeted Antioxidants in the Treatment of Parkinsonism: an Updated Review.Neurotoxicity research · 2022Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Generation of excessive reactive oxygen species (ROS) leads to mitochondrial dysfunction, apoptosis, and necrosis in renal ischemia-reperfusion (IR) injury. Previously we showed that lentiviral vector-mediated overexpression of superoxide dismutase-1 (SOD1) in proximal tubular epithelial cells (LLC-PK(1)) reduced cytotoxicity in an in vitro model of IR injury. Here, we examined the effects of SOD1 overexpression on mitochondrial signaling after ATP depletion-recovery (ATP-DR). To examine the role of mitochondrial ROS, a subset of cells was treated with the mitochondrial antioxidant MitoTEMPO. ATP-DR-mediated increase in mitochondrial calcium, loss of mitochondrial membrane potential, and increase in mitochondrial permeability transition pore (MPTP) were attenuated by SOD1 and MitoTEMPO (P<0.01). SOD1 prevented ATP-DR-induced mitochondrial Bax translocation, although the release of proapoptotic proteins from mitochondria was not prevented by SOD1 alone and required the presence of both SOD1 and MitoTEMPO. SOD1 suppressed the increase in c-jun phosphorylation, suggesting that JNK signaling regulates Bax translocation to mitochondria via ROS. ATP-DR-mediated changes in MPTP and mitochondrial signaling increased necrosis and apoptosis, both of which were partially attenuated by SOD1 and MitoTEMPO. These studies show that SOD1 and MitoTEMPO preserve mitochondrial integrity and attenuate ATP-DR-mediated necrosis and apoptosis.
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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.