Conversely, another study found that the podocyte-specific overexpression of PGC-1α led to the development of a collapsing glomerulopathy phenotype in mice, characterized by podocyte proliferation and dedifferentiation, proteinuria, and renal failure, likely attributable to excessive levels of PGC-1α29. Here, PPARGC1A is linked to lipoprotein glomerulopathy.