Increasing PGC-1α levels in podocytes induce podocyte proliferation and collapsing glomerulopathy development, whereas increasing PGC-1α levels in endothelial cells alter the endothelial function and cause microangiopathy, thus highlighting the cell type-specific role of PGC-1α in the kidney (Figure 2A). This evidence concerns the gene PPARGC1A and lipoprotein glomerulopathy.