Adaptive ER stress promotes mitochondrial remodelling and longevity through PERK-dependent MERCS assembly.

Jose C Casas-Martinez, Qin Xia, Penglin Li, Maria Borja-Gonzalez, Antonio Miranda-Vizuete, Emma McDermott, Peter Dockery, Leo R Quinlan, Katarzyna Goljanek-Whysall, Afshin Samali, Brian McDonagh

Discipline of Physiology, School of Pharmacy and Medical Sciences, University of Galway, Galway, Ireland.Discipline of Physiology, School of Pharmacy and Medical Sciences, University of Galway, Galway, Ireland. · pubmed

Paper

Abstract

The transfer of information and metabolites between the mitochondria and the endoplasmic reticulum (ER) is mediated by mitochondria-ER contact sites (MERCS), allowing adaptations in response to changes in cellular homeostasis. MERCS are dynamic structures essential for maintaining cell homeostasis through the modulation of calcium transfer, redox signalling, lipid transfer, autophagy and mitochondrial dynamics. Under stress conditions such as ER protein misfolding, the Unfolded Protein Response (UPR

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Research summary

The paper claims that adaptive ER stress promotes mitochondrial remodelling and longevity through PERK-dependent MERCS assembly. This research is relevant as it explores mechanisms that may influence cellular homeostasis and longevity, addressing potential root causes of aging through the modulation of mitochondrial dynamics and stress responses.

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