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No off-topic or low-options-content posts.Following them avoids automated filtering or moderator intervention or removal of posts or comments. The guidelines are intended to promote useful & thoughtful conversation. Our findings thus demonstrate a critical protective role of SIRPα in podocyte survival via maintenance of autophagic activity.Q&A New Traders: See the Options Questions Safe Haven thread Mechanistically, podocyte SIRPα strongly reduced Akt/GSK-3β/β-catenin signaling, leading to an increase in autophagic activity. Compared with WT littermates, Sirpa-deficient mice displayed greater age-related podocyte injury and proteinuria and developed more rapid and severe renal injury in various models of experimental nephropathy. Podocyte SIRPα levels were inversely correlated with the severity of podocyte injury and proteinuria but positively with autophagy. Unlike other glomerular cells, podocytes strongly expressed SIRPα, which was, however, downregulated in patients with focal segmental glomerulosclerosis and mice with experimental nephropathy.
Here we report that signal regulatory protein α (SIRPα) plays a key role in promoting podocyte autophagy. How podocytes maintain such a high level of autophagy, however, remains unclear. High autophagic activity in podocytes, terminally differentiated cells that serve as main components of the kidney filtration barrier, is essential for podocyte survival under various challenges.
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