Cellular senescence links mitochondria-ER contacts and aging

Membrane contact sites emerged in the last decade as key players in the integration, regulation and transmission of many signals within cells, with critical impact in multiple pathophysiological contexts. Numerous studies accordingly point to a role for mitochondria-endoplasmic reticulum contacts (MERCs) in modulating aging. Nonetheless, the driving cellular mechanisms behind this role remain unclear. Recent evidence unravelled that MERCs regulate cellular senescence, a state of permanent proliferation arrest associated with a pro-inflammatory secretome, which could mediate MERC impact on aging. Here we discuss this idea in light of recent advances supporting an interplay between MERCs, cellular senescence and aging. This perspective by Ziegler et al. explores the impact of mitochondria-endoplasmic reticulum contacts (MERCs) biology on cellular senescence. The authors also explore the potential impacts of MERCs perturbation and how this relates to the increase in cellular senescence observed in common age-related diseases.