Parkin and PINK1 mitigate STING-induced inflammation.

ABSTRACT: Although serum from patients with Parkinson's disease contains elevated levels of numerous pro-inflammatory cytokines including IL-6, TNF, IL-1β, and IFNγ, whether inflammation contributes to or is a consequence of neuronal loss remains unknown¹. Mutations in parkin, an E3 ubiquitin ligase, and PINK1, a ubiquitin kinase, cause early onset Parkinson's disease^2,3. Both PINK1 and parkin function within the same biochemical pathway and remove damaged mitochondria from cells in culture and in animal models via mitophagy, a selective form of autophagy⁴. The in vivo role of mitophagy, however, is unclear, partly because mice that lack either PINK1 or parkin have no substantial Parkinson's-disease-relevant phenotypes^5-7. Mitochondrial stress can lead to

SUBMITTER: Sliter DA 

PROVIDER: S-EPMC7362342 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature