ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2024
Mitochondrial membrane potential and oxidative stress interact to regulate Oma1-dependent processing of Opa1 and mitochondrial dynamics.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2024. 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.
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- Targeting RuvBL1 disrupts mitochondrial metabolism and structure in hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2026Article
- [Research progress on the mechanism of mitochondrial dynamics in diabetic foot ulcers and its related intervention strategies].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2026Review
- Engrailed-1 potentiates mitochondrial transplant neuroprotection in spinal cord ischemia-reperfusion injury.Communications biology · 2026Article
- FAM162A Is a Key Regulator of Mitochondrial Structure, Dynamics, and Bioenergetics, Driving Cellular Protection and Longevity.Aging cell · 2026Article
- An AI-derived peptide PCa2 suppresses pancreatic cancer growth via modulation of the ErbB/PI3K/AKT/mTOR/MYC signaling axis.Cell communication and signaling : CCS · 2026Article
- Aerobic exercise improve physical endurance and muscle function by ameliorating oxidative stress and modulating mitochondrial dynamics in aged skeletal muscle.Journal of physiology and biochemistry · 2026Article
- Cystinosis and Cellular Energy Failure: Mitochondria at the Crossroads.International journal of molecular sciences · 2026Review
- Protective effect of wild polysaccharides extracted fromFrontiers in pharmacology · 2026Article
- Features of Mitochondrial Dynamics in Different Brain Parts of Patients with Alzheimer's Disease.International journal of molecular sciences · 2025Article
- Cellular cAMP Content and Mitochondrial Profile Define Different Subtypes of Ovarian Cancer Cells.International journal of molecular sciences · 2025Article
- NAD+-Boosters Improve Mitochondria Quality Control In Parkinson's Disease Models Via Mitochondrial UPR.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Optineurin deficiency disrupts phosphorylated tau proteostasis and clusterin expression in human neurons.Acta neuropathologica communications · 2025Article
- The role of cardiolipin in mitochondrial dynamics and quality control in neuronal ischemia/reperfusion injury.Cell death & disease · 2025Review
- Agent-based modeling of neuronal mitochondrial dynamics using intrinsic variables of individual mitochondria.iScience · 2025Article
- A New Perspective on the Role of Alterations in Mitochondrial Proteins Involved in ATP Synthesis and Mobilization in Cardiomyopathies.International journal of molecular sciences · 2025Review
- Regulation of mitochondrial dynamics in cardiomyocytes: implications for cardiac health and disease.Frontiers in cell and developmental biology · 2025Review
- Analysis of neuronal cardiolipin and monolysocardiolipin from biological samples with cyclic ion mobility mass spectrometry.Frontiers in physiology · 2025Article
- Off-target effects of mitochondrial oxidative phosphorylation inhibitors are common and can compromise the viability of cultured cells.Mitochondrial communications · 2025Article
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Abstract
Mitochondrial form and function are regulated by the opposing forces of mitochondrial dynamics: fission and fusion. Mitochondrial dynamics are highly active and consequential during neuronal ischemia/reperfusion (I/R) injury. Mitochondrial fusion is executed at the mitochondrial inner membrane by Opa1. The balance of long (L-Opa1) and proteolytically cleaved short (S-Opa1) isoforms is critical for efficient fusion. Oma1 is the predominant stress-responsive protease for Opa1 processing. In neuronal cell models, we assessed Oma1 and Opa1 regulation during mitochondrial stress. In an immortalized mouse hippocampal neuron line (HT22), Oma1 was sensitive to mitochondrial membrane potential depolarization (rotenone, FCCP) and hyperpolarization (oligomycin). Further, oxidative stress was sufficient to increase Oma1 activity and necessary for depolarization-induced proteolysis. We generated Oma1 knockout (KO) HT22 cells that displayed normal mitochondrial morphology and fusion capabilities. FCCP-induced mitochondrial fragmentation was exacerbated in Oma1 KO cells. However, Oma1 KO cells were better equipped to perform restorative fusion after fragmentation, presumably due to preserved L-Opa1. We extended our investigations to a combinatorial stress of neuronal oxygen-glucose deprivation and reoxygenation (OGD/R), where we found that Opa1 processing and Oma1 activation were initiated during OGD in an ROS-dependent manner. These findings highlight a novel dependence of Oma1 on oxidative stress in response to depolarization. Further, we demonstrate contrasting fission/fusion roles for Oma1 in the acute response and recovery stages of mitochondrial stress. Collectively, our results add intersectionality and nuance to the previously proposed models of Oma1 activity.
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