ArticleJournal of extracellular biology2022
Defective mitochondria-lysosomal axis enhances the release of extracellular vesicles containing mitochondrial DNA and proteins in Huntington's disease.
Article in Journal of extracellular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Mitochondrial quality control in health and disease: Updates 2026.Chinese medical journal · 2026Review
- Salivary protein macromolecules as diagnostic and therapeutic biomarkers linking oral health and neurodegenerative diseases-emerging mechanisms and future perspectives.Inflammopharmacology · 2026Review
- Two Routes for Removing Unhealthy Mitochondria: Degradation and Secretion.Circulation research · 2026Review
- Mitochondrial DNA: a molecular switch driving sterile neuroinflammation.Translational neurodegeneration · 2026Review
- Beyond Decellularization: Remnant Mitochondrial DNA Can Act as Hidden Damage-Associated Molecular Pattern.Bioengineering (Basel, Switzerland) · 2026Article
- The profiling of extracellular vesicle subtypes in Huntington's disease brains identifies Alix as a novel marker of neuropathology.Acta neuropathologica communications · 2025Article
- The Immunogenic Role of Self-DNA in T Cell Immunity.Clinical reviews in allergy & immunology · 2025Review
- Gangliosides modulate the secretion of extracellular vesicles and their misfolded protein cargo.Science advances · 2025Article
- Mitochondrial Quality Control in Neurodegeneration and Cancer: A Common Denominator, Distinct Therapeutic Challenges.International journal of molecular sciences · 2025Review
- Multiomics analysis to evaluate the enrichment of extracellular vesicles from human plasma.Journal of lipid research · 2025Article
- Extracellular Vesicles for Clinical Diagnostics: From Bulk Measurements to Single-Vesicle Analysis.ACS nano · 2025Review
- Is the Voltage-Dependent Anion Channel a Major Player in Neurodegenerative Diseases?International journal of molecular sciences · 2025Review
- Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025Review
- Extracellular vesicles: new horizons in neurodegeneration.EBioMedicine · 2025Review
- Mitochondrial DNA leakage: underlying mechanisms and therapeutic implications in neurological disorders.Journal of neuroinflammation · 2025Review
- Imaging Mitochondrial Axonal Transport in Human Induced Pluripotent Stem Cell-Derived Neurons.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Mitochondria break free: Mitochondria-derived vesicles in aging and associated conditions.Ageing research reviews · 2024Review
- Motor skill learning modulates striatal extracellular vesicles' content in a mouse model of Huntington's disease.Cell communication and signaling : CCS · 2024Article
- Extracellular release in the quality control of the mammalian mitochondria.Journal of biomedical science · 2023Review
- The Tricky Connection between Extracellular Vesicles and Mitochondria in Inflammatory-Related Diseases.International journal of molecular sciences · 2023Review
Corrections and comments
- Erratum issuedCorrection to2025
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial and autophagy dysfunction are mechanisms proposed to be involved in the pathogenesis of several neurodegenerative diseases. Huntington's disease (HD) is a progressive neurodegenerative disorder associated with mutant Huntingtin-induced abnormalities in neuronal mitochondrial dynamics and quality control. Former studies suggest that the removal of defective mitochondria may be compromised in HD. Mitochondrial quality control (MQC) is a complex, well-orchestrated pathway that can be compromised through mitophagy dysregulation or impairment in the mitochondria-lysosomal axis. Another mitochondrial stress response is the generation of mitochondrial-derived vesicles that fuse with the endolysosomal system and form multivesicular bodies that are extruded from cells as extracellular vesicles (EVs). In this work, we aimed to study the presence of mitochondrial components in human EVs and the relation to the dysfunction of both mitochondria and the autophagy pathway. We comprehensively characterized the mitochondrial and autophagy alterations in premanifest and manifest HD carriers and performed a proteomic and genomic EVs profile. We observed that manifest HD patients exhibit mitochondrial and autophagy impairment associated with enhanced EVs release. Furthermore, we detected mitochondrial DNA and proteins in EVs released by HD cells and in neuronal-derived EVs including VDAC-1 and alpha and beta subunits of ATP synthase F1. HD-extracellular vesicles transport higher levels of mitochondrial genetic material in manifest HD patients, suggesting an alternative pathway for the secretion of reactive mitochondrial components. This study provides a novel framework connecting EVs enhanced release of mitochondrial components to mitochondrial and lysosomal dysfunction in HD.
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