Podocytes and autophagy: a potential therapeutic target in lupus nephritis
| العنوان: | Podocytes and autophagy: a potential therapeutic target in lupus nephritis |
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| المؤلفون: | Xu-jie Zhou, Hong Zhang, Daniel J. Klionsky |
| المصدر: | Autophagy. 15:908-912 |
| بيانات النشر: | Informa UK Limited, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | 0301 basic medicine, ATG5, Lupus nephritis, mTORC1, Biology, Kidney, Autophagy-Related Protein 5, Mice, 03 medical and health sciences, Phagocytosis, Autophagy, medicine, Animals, Humans, Lupus Erythematosus, Systemic, Molecular Targeted Therapy, Molecular Biology, Inflammation, Sirolimus, Systemic lupus erythematosus, 030102 biochemistry & molecular biology, Podocytes, Cell Biology, BECN1, medicine.disease, Lupus Nephritis, 030104 developmental biology, Commentary, IRGM, Cancer research, Microtubule-Associated Proteins, MAP1LC3B |
| الوصف: | 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. Abbreviations: ALB: albumin; ARHGDIB: Rho GDP dissociation inhibitor beta; APOL1: apolipoprotein L1; ATG5: autophagy related 5; ATG7: autophagy related 7; ATG16L2: autophagy related 16 like 2; BECN1: beclin 1; CDKN1B: cyclin dependent kinase inhibitor 1B; CLEC16A, C-type lectin domain containing 16A; CYBB: cytochrome b-245 beta chain; DC: dendritic cell; DRAM1: DNA damage regulated autophagy modulator 1; eQTL: expression quantitative trait loci; GWAS: genome-wide association study; IFNA: interferon alpha; IRGM: immunity related GTPase M; LRRK2: leucine rich repeat kinase 2; MAP1LC3B: microtubule associated protein 1 light chain 3 beta; MTMR3: myotubularin related protein 3; LAP” LC3-associated phagocytosis; LN: lupus nephritis; NOD: non-obese diabetic; NPHS2: NPHS2, podocin; PBMC: peripheral blood mononuclear cell; RUBCN: rubicon autophagy regulator; SLE: systemic lupus erythematosus. |
| تدمد: | 1554-8635 1554-8627 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e9329cbf1bcc132c0af4e22a8d6c18ddTest https://doi.org/10.1080/15548627.2019.1580512Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....e9329cbf1bcc132c0af4e22a8d6c18dd |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15548635 15548627 |
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