ArticleCells2019
Inhibition of the Fission Machinery Mitigates OPA1 Impairment in Adult Skeletal Muscles.
Article in Cells, 2019. 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, 86 citations in OpenAlex.
- Review
- Exercise-mediated regulation of mitochondrial dynamics in aging muscle: implications for mitochondrial diseases.Molecular and cellular biochemistry · 2026Review
- Role of mitochondrial dysfunction in muscle wasting in cancer cachexia: a narrative review.Journal of translational medicine · 2026Review
- Mitochondria-associated endoplasmic reticulum membranes: Emerging regulators of cardiac microvascular ischemia/reperfusion injury (Review).International journal of molecular medicine · 2026Review
- Leveraging mitochondrial stress to improve healthy aging.Sports medicine and health science · 2026Review
- Endoplasmic reticulum autophagy in inflammatory diseases.Frontiers in immunology · 2026Review
- Alterations in peroxisome-mitochondria interplay in skeletal muscle accelerate muscle dysfunction.Nature communications · 2025Article
- Optic Atrophy 1: The Conductor of Cellular Harmony and Age-Related Pathologies.Aging and disease · 2025Review
- The Balance of MFN2 and OPA1 in Mitochondrial Dynamics, Cellular Homeostasis, and Disease.Biomolecules · 2025Review
- Myokines: metabolic regulation in obesity and type 2 diabetes.Life metabolism · 2024Review
- The role of mitochondrial dynamics and mitophagy in skeletal muscle atrophy: from molecular mechanisms to therapeutic insights.Cellular & molecular biology letters · 2024Review
- ATF4-dependent and independent mitokine secretion from OPA1 deficient skeletal muscle in mice is sexually dimorphic.Frontiers in endocrinology · 2024Article
- Females display relatively preserved muscle quality compared with males during the onset and early stages of C26-induced cancer cachexia.Journal of applied physiology (Bethesda, Md. : 1985) · 2023Article
- Intracellular to Interorgan Mitochondrial Communication in Striated Muscle in Health and Disease.Endocrine reviews · 2023Review
- The pre-conception maternal exposure to Sofosbuvir affects the mitochondrial biogenesis in prenatal fetal tissues: Experimental study on rats.Molecular medicine (Cambridge, Mass.) · 2023Article
- The Role of Mitochondria in Mediation of Skeletal Muscle Repair.Muscles (Basel, Switzerland) · 2023Review
- Ageing of skeletal muscle extracellular matrix and mitochondria: finding a potential link.Annals of medicine · 2023Review
- From mitochondria to sarcopenia: role of 17β-estradiol and testosterone.Frontiers in endocrinology · 2023Review
- The mediating role of inflammaging between mitochondrial dysfunction and sarcopenia in aging: a review.American journal of clinical and experimental immunology · 2023Review
- MicroRNAs as the Sentinels of Redox and Hypertrophic Signalling.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The maintenance of muscle mass and its ability to function relies on a bioenergetic efficient mitochondrial network. This network is highly impacted by fusion and fission events. We have recently shown that the acute deletion of the fusion protein Opa1 induces muscle atrophy, systemic inflammatory response, precocious epithelial senescence, and premature death that are caused by muscle-dependent secretion of FGF21. However, both fusion and fission machinery are suppressed in aging sarcopenia, cancer cachexia, and chemotherapy-induced muscle wasting. We generated inducible muscle-specific Opa1 and Drp1 double-knockout mice to address the physiological relevance of the concomitant impairment of fusion and fission machinery in skeletal muscle. Here we show that acute ablation of Opa1 and Drp1 in adult muscle causes the accumulation of abnormal and dysfunctional mitochondria, as well as the inhibition of autophagy and mitophagy pathways. This ultimately results in ER stress, muscle loss, and the reduction of force generation. However, the simultaneous inhibition of the fission protein Drp1 when Opa1 is absent alleviates FGF21 induction, oxidative stress, denervation, and inflammation rescuing the lethal phenotype of Opa1 knockout mice, despite the presence of any muscle weakness. Thus, the simultaneous inhibition of fusion and fission processes mitigates the detrimental effects of unbalanced mitochondrial fusion and prevents the secretion of pro-senescence factors.
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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.