Fig. 7: Schematic model of the role of BMPR2 in the inhibition of fatty acid metabolism and induction of cell death.
From: BMPR2 promotes fatty acid oxidation and protects white adipocytes from cell death in mice
BMPR2 signaling facilitates lipolysis by activating phosphorylation and dynamics of perilipin, thus guaranteeing the availability of fatty acid for β-oxidation (FAO) and oxidative phosphorylation (OXPHOS) through electron transport chain (ETC). BMPR2 deficiency disrupts this action, leading to the failure of OXPHOS, and activates mitochondria-mediated apoptosis in adipocytes when adipocytes were stimulated by TNFα. Meanwhile, deficiency of lipolysis leads to hypertrophy of adipocytes and subsequent pyroptosis and inflammation, among which elevation of TNFα is prominent. TNFα in turn poses more pressure on adipocyte, accelerating the process of cell death. BMPR2 deficiency thus renders the white adipocytes vulnerable to cell death. FFA free fatty acid, TAG triacylglyceride.
