ArticleNeurology research international2013
Mitochondrial fusion proteins and human diseases.
Article in Neurology research international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed.
- Cell-Type-Specific Calibration of Mitochondrial Ubiquitination in Stem Cell Fate Decisions.Stem cell reviews and reports · 2026Review
- Inhibition of RBM25 preserves cardiac mitochondrial homeostasis and attenuates ischemic heart failure.Journal of molecular histology · 2026Article
- Mitochondria in health and disease: cellular powerhouses, signaling centers, and drivers of dysfunction.Frontiers in cell and developmental biology · 2026Review
- Review
- Mitochondrial Dysfunction in Endothelial Cells: A Key Driver of Organ Disorders and Aging.Antioxidants (Basel, Switzerland) · 2025Review
- Mapping mitochondrial morphology and function: COX-SBFSEM reveals patterns in mitochondrial disease.Communications biology · 2025Article
- Integrating network pharmacology and experimental validation to investigate the mechanism of Gualou Xiebai Banxia decoction against myocardial ischemia.Frontiers in cardiovascular medicine · 2025Article
- ISGylation of DRP1 closely balances other post-translational modifications to mediate mitochondrial fission.Cell death & disease · 2024Article
- Nicotinic receptors in airway disease.American journal of physiology. Lung cellular and molecular physiology · 2024Review
- Mitochondrial hyperfusion induces metabolic remodeling in lung endothelial cells by modifying the activities of electron transport chain complexes I and III.Free radical biology & medicine · 2024Article
- Novel Relationship between Mitofusin 2-Mediated Mitochondrial Hyperfusion, Metabolic Remodeling, and Glycolysis in Pulmonary Arterial Endothelial Cells.International journal of molecular sciences · 2023Article
- Nicotine affects mitochondrial structure and function in human airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Mitochondria as central hubs in synaptic modulation.Cellular and molecular life sciences : CMLS · 2023Review
- Novel insights into the involvement of mitochondrial fission/fusion in heart failure: From molecular mechanisms to targeted therapies.Cell stress & chaperones · 2023Review
- Impaired mitochondrial dynamics and removal of the damaged mitochondria in diabetic retinopathy.Frontiers in endocrinology · 2023Article
- Mitochondrial Membranes and Mitochondrial Genome: Interactions and Clinical Syndromes.Membranes · 2022Review
- Adhesion response of filopodia to an AFM lateral detachment force and functional changes after centrifugation of cells grown on nanoporous titanium.Materials today. Bio · 2022Article
- Mitochondrial Fragmentation in a High Homocysteine Environment in Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2022Article
- Regulation of mitochondrial fission by GIPC-mediated Drp1 retrograde transport.Molecular biology of the cell · 2022Article
- Mitochondrial Dynamics in the Metabolic Memory of Diabetic Retinopathy.Journal of diabetes research · 2022Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are highly dynamic, complex organelles that continuously alter their shape, ranging between two opposite processes, fission and fusion, in response to several stimuli and the metabolic demands of the cell. Alterations in mitochondrial dynamics due to mutations in proteins involved in the fusion-fission machinery represent an important pathogenic mechanism of human diseases. The most relevant proteins involved in the mitochondrial fusion process are three GTPase dynamin-like proteins: mitofusin 1 (MFN1) and 2 (MFN2), located in the outer mitochondrial membrane, and optic atrophy protein 1 (OPA1), in the inner membrane. An expanding number of degenerative disorders are associated with mutations in the genes encoding MFN2 and OPA1, including Charcot-Marie-Tooth disease type 2A and autosomal dominant optic atrophy. While these disorders can still be considered rare, defective mitochondrial dynamics seem to play a significant role in the molecular and cellular pathogenesis of more common neurodegenerative diseases, for example, Alzheimer's and Parkinson's diseases. This review provides an overview of the basic molecular mechanisms involved in mitochondrial fusion and focuses on the alteration in mitochondrial DNA amount resulting from impairment of mitochondrial dynamics. We also review the literature describing the main disorders associated with the disruption of mitochondrial fusion.
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Registered trials
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