https://www.tandfonline.com/doi/abs/10.1080/15548627.2019.1580512?journalCode=kaup20
https://www.ncbi.nlm.nih.gov/pubmed/30755075?dopt=Abstract
Podocytes and autophagy: A potential therapeutic target in lupus nephritis.
Autophagy
Related Articles
Podocytes and autophagy: A potential therapeutic target in lupus nephritis.
Autophagy. 2019 Feb 13;:
Authors: Zhou XJ, Klionsky DJ, Zhang H
Abstract
Recent studies suggest that defects in macroautophagy/autophagy contribute to the pathogenesis of systemic lupus erythamatosus (SLE), especially in adaptive immunity. The occurrence and progression of lupus nephritis (LN) is the end result of complex interactions between regulation of immune responses and pathological process by renal resident cells, but there is still a lot of missing information for establishing the role of autophagy in the pathogenesis of LN, and as a therapy target. In our recent study, we observed that autophagy is activated in LN, especially in podocytes. Based on in vitro assays, many of the most important mediators of the disease-patients’ sera, patients’ IgG and IFNA/IFN-α-can induce autophagy in both murine and human podocytes, by reactive oxygen species production or MTORC1 inhibition; autophagy activation negatively associates with podocyte injury. With regard to intervention, autophagy activators can protect against podocyte injury, whereas autophagy inhibitors aggravate injury. Taken together, our findings suggest that podocyte autophagy is involved in lupus renal protection and may be a therapeutic target. These data shed new light on the role of rapamycin and autophagy inducers in the treatment of SLE.
PMID: 30755075 [PubMed – as supplied by publisher]
PubMed:30755075