Damage to podocytes is a central pathomechanism of proteinuric kidney disease. However,
it is not fully understood how podocyte injury evolves to progressive glomerulopathies such
as FSGS or collapsing glomerulopathy. In particular, the role of parietal epithelial cells
remains controversial. Here, we show that adriamycin induces DNA damage and podocyte
lysis in mice without evidence of autophagy, endoplasmic reticulum stress, or necroptosis.
After extensive podocyte loss, activated parietal cells mediated tuft re-epithelialization by two …