ArticleFrontiers in cell and developmental biology2020
OPA1-Exon4b Binds to mtDNA D-Loop for Transcriptional and Metabolic Modulation, Independent of Mitochondrial Fusion.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Association Between Mitochondrial DNA Copy Number and Head and Neck Squamous Cell Carcinoma: A Systematic Review and Dose-Response Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2021Pooled it
- MitoPerturb-Seq identifies gene-specific single-cell responses to mitochondrial DNA depletion and heteroplasmy.Nature structural & molecular biology · 2026Article
- Longitudinal Analysis of Mitochondrial D-Loop Methylation and Copy Number in Peripheral Blood: Epigenetic Signatures of Alzheimer's Disease Progression and Aging.International journal of molecular sciences · 2026Article
- Diagnostic and therapeutic innovations in myocardial infarction: a focus on mitochondrial dysfunction.Frontiers in cardiovascular medicine · 2026Review
- Subcellular Stress Markers in Epithelial Ovarian Cancer.International journal of molecular sciences · 2025Review
- CRISPRa-Mediated Increase of OPA1 Expression in Dominant Optic Atrophy.International journal of molecular sciences · 2025Article
- Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Bringing together but staying apart: decisive differences in animal and fungal mitochondrial inner membrane fusion.Biological reviews of the Cambridge Philosophical Society · 2025Review
- Optic Atrophy 1: The Conductor of Cellular Harmony and Age-Related Pathologies.Aging and disease · 2025Review
- OPA1 and disease-causing mutants perturb mitochondrial nucleoid distribution.Cell death & disease · 2024Article
- Article
- Human retinal organoids with an OPA1 mutation are defective in retinal ganglion cell differentiation and function.Stem cell reports · 2024Article
- Modelling autosomal dominant optic atrophy associated with OPA1 variants in iPSC-derived retinal ganglion cells.Human molecular genetics · 2022Article
- Metabolic reprogramming in the OPA1-deficient cells.Cellular and molecular life sciences : CMLS · 2022Article
- CRISPR-Cas9 correction ofMolecular therapy. Nucleic acids · 2021Article
- Opa1 Deficiency Promotes Development of Retinal Vascular Lesions in Diabetic Retinopathy.International journal of molecular sciences · 2021Article
- Remodeling of Mitochondrial Plasticity: The Key Switch from NAFLD/NASH to HCC.International journal of molecular sciences · 2021Review
- Review
- Opa1 Reduces Hypoxia-Induced Cardiomyocyte Death by Improving Mitochondrial Quality Control.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Optic Atrophy 1 (OPA1) has well-established roles in both mitochondrial fusion and apoptotic crista remodeling and is required for the maintenance and distribution of mitochondrial DNA (mtDNA), which are essential for energy metabolism. However, the relationship between OPA1 and mitochondrial metabolism and the underlying mechanisms remain unclear. Here, we show that OPA1-Exon4b modulates mitochondrial respiration and rescues inner mitochondrial membrane potential (Δψm), independent of mitochondrial fusion. OPA1-Exon4b is required for the maintenance of normal TFAM distribution and enhances mtDNA transcription by binding the D-loop of mtDNA. Finally, we show that mRNA levels of OPA1 isoforms containing Exon4b are specifically downregulated in hepatocellular carcinoma (HCC), leading to a reduction in Δψm. Thus, our study demonstrates a novel mitochondrial functional self-recovery pathway involving enhanced mtDNA transcription-mediated recovery of mitochondrial respiratory chain proteins. This mitochondrial fusion-independent pathway may contribute to mitochondrial multi-functional switches in tumorigenesis.
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