Adipose-Derived Mesenchymal Stem Cell Exosomes Attenuate Oxygen-Glucose Deprivation-Induced Cochlear Damage by Inducing Autophagy-Associated Signaling.
Lin YC., Lin YY., Chen HK., Chen HC., Wang CH., Hung CM.
Animal Study on Hair & Scalp, published in Int J Mol Sci (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Int J Mol Sci (2026)
- Country
- Switzerland
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 42511454
- DOI
- 10.3390/ijms27146108
Abstract (original English)
Ischemia plays a critical role in the pathogenesis of sensorineural hearing loss through the induction of severe cochlear apoptosis and mitochondrial dysfunction. Exosomes derived from adipose-derived mesenchymal stem cells (ADMSC-Exo) have robust protective effects under non-otologic ischemic conditions. However, their otoprotective effects remain unclear. This study aimed to investigate the protective effects of human ADMSC-Exo against cochlear damage and mitochondrial dysfunction under oxygen-glucose deprivation (OGD), an in vitro and ex vivo model of cochlear ischemia. ADMSC-Exo attenuated OGD-induced cytotoxicity and apoptosis in HEI-OC1 cells and reduced the OGD-induced loss of cochlear hair cells in the organ of Corti explants. OGD caused a decrease in mitochondrial mass and mitochondrial membrane potential depolarization and impaired mitochondrial respiration in auditory cells. ADMSC-Exo preserved mitochondrial integrity and improved mitochondrial bioenergetic function following OGD exposure. These effects were accompanied by increased LC3-II conversion and formation of autolysosome-like structures and elevated expression of PINK1 and Parkin, indicating the activation of autophagy and mitophagy-related protective mechanisms. Importantly, 3-methyladenine, an autophagy inhibitor, attenuated the cytoprotective effect of ADMSC-Exo, supporting the involvement of autophagy in
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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