Summary
Ultimately, the common final pathway of any glomerular disease is podocyte effacement,
podocyte loss, and, eventually, glomerular scarring. There has been a long-standing
debate on the underlying mechanisms for podocyte depletion, ranging from necrosis
and apoptosis to detachment of viable cells from the glomerular basement membrane.
However, this debate still continues because additional pathways of programmed cell
death have been reported in recent years. Interestingly, viable podocytes can be isolated
out of the urine of proteinuric patients easily, emphasizing the importance of podocyte
detachment in glomerular diseases. In contrast, detection of apoptosis and other pathways
of programmed cell death in podocytes is technically challenging. In fact, we still
are lacking direct evidence showing, for example, the presence of apoptotic bodies
in podocytes, leaving the question unanswered as to whether podocytes undergo mechanisms
of programmed cell death. However, understanding the mechanisms leading to podocyte
depletion is of particular interest because future therapeutic strategies might interfere
with these to prevent glomerular scarring. In this review, we summarize our current
knowledge on podocyte cell death, the different molecular pathways and experimental
approaches to study these, and, finally, focus on the mechanisms that prevent the
onset of programmed cell death.
Keywords
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☆Financial disclosure and conflict of interest statements: none.
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