Endoplasmic Reticulum Stress Inhibition Promotes Mitophagy via Miro1 Reduction to Rescue Mitochondrial Dysfunction and Protect Dopamine Neurons in Parkinson's Disease.

ABSTRACT: Both mitochondrial dysfunction and endoplasmic reticulum stress (ERS) have been implicated in the pathogenesis of Parkinson's disease (PD). However, the underlying regulatory mechanisms between ERS and mitochondrial dysfunction remain unclear. In the present study, we found that an in vitro model of Parkinson's disease (PD) induced by methyl-4-phenylpyridine (MPP⁺) showed increased intracellular peroxidation, leading to a significant increase in ERS. ER staining and immunofluorescence analysis of ERS-related proteins verified the presence of ERS, whereas transmission electron microscopy (TEM) showed complete depletion of ER. Notably, treatment with 4-phenylbutyric acid (4-PBA) to suppress ERS reduced apoptosis and concurrently reversed the ER micromorphology. Furthermore, 4-PBA

SUBMITTER: Wen Y 

PROVIDER: S-EPMC12122992 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature