Excessive ER-mitochondria coupling: A DRP1-driven mechanism underlying mitochondrial dysfunction and impaired autophagy in stress-induced depression-like behavior in mice - PubMed
5 hours ago
- #Autophagy
- #Depression
- #Mitochondrial Dysfunction
- Excessive ER-mitochondria coupling driven by DRP1 leads to mitochondrial dysfunction and impaired autophagy in stress-induced depression-like behavior in mice.
- Mitochondrial dynamics regulated by DNM1L/DRP1 are critical for neuronal homeostasis, and their dysregulation may contribute to cellular impairment in depression.
- Disruption of mitochondrial-endoplasmic reticulum contact sites (MERCs) by DRP1 activation results in mitochondrial dysfunction and depressive-like behaviors.
- Inhibiting the MERC tethering protein GRP75 or enhancing mitophagy pharmacologically alleviates neuronal and behavioral deficits in depression models.
- The study highlights the importance of ER-mitochondrial crosstalk in depression and suggests potential therapeutic targets for stress-related disorders.