Fig. 3. ATGL effects in redox homoeostasis.

ATGL-mediated release of free fatty acids (FFAs) from lipid droplets (LDs) is a source of mitochondrial reactive oxygen species (ROS). The ATGL-PPAR-α axis mitigates oxidative stress favouring the expression of antioxidant enzymes in (1) skeletal muscle (i.e., SOD2 and γ-GCL, two downstream targets of NFE2L2) and in (2) intestines (i.e., GSTT1, GSTK1 and GSTM3). ATGL activity impairs the expression of catalytic subunits of the NADPH oxidase complex in (3) cardiac muscle (i.e., CYBB, codifying for NOX2 protein, and NOX4) and in (4) macrophages (i.e., NOX1). The influence of PPAR-α in these latter events has been not investigated, yet