VIDEO: Interferon-induced APOL1 over-expression linked to autophagic dysfunction

SAN DIEGO — At the American College of Rheumatology Annual Meeting, Ashira Blazer, MD, discussed a study in which the researchers hypothesized that cytokine-induced risk variant expression impairs autophagy, favoring pore formation endothelial cells, implicating endothelial dysfunction as a cause for broader organ damage. According to Blazer, interferon gamma increases both ancestral and variant APOL1 intracellular accumulation in cultured endothelial cells across genotype. Among risk variant carrying endothelial cells, this results in abnormal autophagy, angiogenesis and mitochondrial energy production, contributing to endothelial dysfunction.