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Polycystin-2 functions as a calcium leak channel under endoplasmic reticulum stress to protect against myocardial ischemia.
Cell Reports · · Journal Article
Vuchkovska, Paluru + more
Abstract ↗AI summary
The abstract is read at the publisher; the summary is JClub's.
Polycystin-2 acts as a PERK-dependent calcium leak channel under ER stress to protect against myocardial infarction in mice.
- Why it matters: Understanding how ER stress influences calcium signaling is crucial because unresolved ER stress worsens diseases like myocardial infarction, but the specific calcium sources involved are unclear.
- What they did: The study examined cardiomyocytes and MI models, finding that ER-localized polycystin-2 is upregulated during MI and facilitates an ER calcium leak at MERCs, requiring PERK phosphorylation.
- The result: This reveals that polycystin-2 provides mitochondrial calcium under ER stress in a PERK-dependent manner, and its upregulation may serve as a cardioprotective mechanism during MI.
The findingWhy it mattersWhat they didThe result