Excessive EFHD1-dependent ER-mitochondrial contacts drive a maladaptive antiviral response in metabolic liver disease
It is shown that EFHD1, a Ca2+-dependent actin cross-linker, stabilizes endoplasmic reticulum–mitochondria contact sites (ERMCS) by detecting spatiotemporal coincidence of interorganellar proximity and ER Ca2+ release, and suggested EFHD1 inhibition as a therapeutic strategy.