Xi Fang

This study shows that targeting ALCAT1 improves cardiac function in Barth syndrome by restoring mitochondrial quality control through phosphatidylinositol signaling and lysosomal function, without correcting cardiolipin abnormalities.

This study shows that saturated cardiolipins (CLsat) disrupt inner mitochondrial membrane structure and function, contributing to mitochondrial dysfunction in Barth syndrome.

This study identifies Kindlin-2-Moesin interaction as a regulator of sprouting angiogenesis by modulating endothelial membrane tension and VEGF signaling.

This study characterizes acute tissue and functional deficits in a pig model of ischemic stroke to identify treatment targets and inform therapeutic development.