Autophagy in Podocytes

Abstract

<b><i>Background:</i></b> Podocyte injury and loss, caused by a variety of insults, is a common and determining factor for the progression of glomerular diseases. Being postmitotic and highly differentiated, podocytes have no or a very limited ability to proliferate or regenerate. Thus, understanding the mechanisms that help maintain and defend podocytes is of great importance. Autophagy is a cellular process by which cytoplasmic cargos are sequestered within autophagosomes and then delivered to lysosomes for degradation and turnover. Recent research has highlighted an important role of autophagy in the maintenance of cellular homeostasis under physiological and pathological conditions. <b><i>Summary:</i></b> A high basal level of autophagy is a characteristic hallmark of differentiated podocytes, which may contribute critically to the structural and functional integrity of the cells. Autophagy is also essential for long-term podocyte homeostasis in aging, protecting podocytes against cellular degeneration and age-related kidney diseases. In glomerular diseases, alteration of autophagic activity may be an adaptive and protective mechanism against podocyte injury and disease progression. Recent studies have further suggested an intriguing and unique interplay between mTOR signaling and autophagy in podocytes. <b><i>Key Messages:</i></b> Altogether, these findings unveil an emerging role of autophagy in the physiology and pathology of podocytes. Further work should elucidate the regulatory mechanism of autophagy in podocytes, determine its pathophysiological role in various kidney diseases, and test autophagy-targeting therapies.