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CD36 aggravates podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy in lupus nephritis.
Lv, Fu; He, Yingxin; Xu, Hongde; Li, Yongchun; Han, Lipei; Yan, Lijie; Lang, Hui; Zhao, Yafei; Zhao, Zhanzheng; Qi, Yuanyuan.
Afiliación
  • Lv F; Nephrology Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Henan, 450052, China.
  • He Y; School of Pharmaceutical Sciences, Zhengzhou University, 100 Ke xue Avenue, Zhengzhou, Henan, 450001, China.
  • Xu H; School of Pharmaceutical Sciences, Zhengzhou University, 100 Ke xue Avenue, Zhengzhou, Henan, 450001, China.
  • Li Y; School of Pharmaceutical Sciences, Zhengzhou University, 100 Ke xue Avenue, Zhengzhou, Henan, 450001, China.
  • Han L; Nephrology Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Henan, 450052, China.
  • Yan L; School of Pharmaceutical Sciences, Zhengzhou University, 100 Ke xue Avenue, Zhengzhou, Henan, 450001, China.
  • Lang H; School of Pharmaceutical Sciences, Zhengzhou University, 100 Ke xue Avenue, Zhengzhou, Henan, 450001, China.
  • Zhao Y; Nephrology Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Henan, 450052, China.
  • Zhao Z; Nephrology Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Henan, 450052, China. zhanzhengzhao@zzu.edu.cn.
  • Qi Y; Nephrology Hospital, the First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Henan, 450052, China. qqyyiillyy@126.com.
Cell Death Dis ; 13(8): 729, 2022 08 23.
Article en En | MEDLINE | ID: mdl-35999224
A major cause of proteinuria in lupus nephritis (LN) is podocyte injury, and determining potential therapeutic targets to prevent podocyte injury is important from a clinical perspective in the treatment of LN. CD36 is involved in podocyte injury in several glomerulopathies and was reported to be a vital candidate gene in LN. Here, we determined the role of CD36 in the podocyte injury of LN and the underlying mechanisms. We observed that CD36 and NLRP3 (NLR family pyrin domain containing 3) were upregulated in the podocytes of lupus nephritis patients and MRL/lpr mice with renal impairment. In vitro, CD36, NLRP3 inflammasome, and autophagy were elevated accompanied with increased podocyte injury stimulated by IgG extracted from lupus nephritis patients compared that from healthy donors. Knocking out CD36 with the CRISPR/cas9 system decreased the NLRP3 inflammasome levels, increased the autophagy levels and alleviated podocyte injury. By enhancing autophagy, NLRP3 inflammasome was decreased and podocyte injury was alleviated. These results demonstrated that, in lupus nephritis, CD36 promoted podocyte injury by activating NLRP3 inflammasome and inhibiting autophagy by enhancing which could decrease NLRP3 inflammasome and alleviate podocyte injury.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Nefritis Lúpica / Podocitos Límite: Animals Idioma: En Revista: Cell Death Dis Año: 2022 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Nefritis Lúpica / Podocitos Límite: Animals Idioma: En Revista: Cell Death Dis Año: 2022 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido