ISSN 1674-3865  CN 21-1569/R
主管:国家卫生和计划生育委员会
主办:中国医师协会
   辽宁省基础医学研究所
   辽宁中医药大学附属医院

Chinese Pediatrics of Integrated Traditional and Western Medicine ›› 2025, Vol. 17 ›› Issue (5): 397-401.doi: 10.20274/j.cnki.issn.1674-3865.2025.05.007

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Study on the mechanism of action of renal resident cells in lupus nephritis based on NF-κB

Hongxun HUANG1, Weiwei LI2()   

  1. 1.Guangxi University of Traditional Chinese Medicine, Nanning 530022,China
    2.The First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine, Nanning 530022,China
  • Received:2025-03-14 Revised:2025-04-25 Published:2025-10-25 Online:2025-10-25
  • Contact: Weiwei LI E-mail:13878161612@163.com

Abstract:

Lupus nephritis (LN) is an immunocomplex nephritis caused by systemic lupus erythematosus (SLE) involving the kidneys. The main manifestation of LN is the deposition of autoantibodies and their immunocomplexes in the kidneys, which triggers a chronic inflammatory infiltration and the gradual destruction of the structure and function of the kidneys. The renal resident cells play a crucial role in this process. Recent studies have shown that nuclear factor-kappa B (NF-κB) can regulate the gene expression of multiple cytokines, growth factors and adhesion molecules in the progression of inflammation, such as the expression of monocyte chemoattractant protein-1 and granulocyte-macrophage colony-stimulating factors in mesangium and glomerular epithelial cells. NF-κB is closely related to the development of LN and plays a unique role in targeting and regulating the biological responses of renal resident cells, including renal mesangial cells, podocytes and tubular epithelial cells. Against this background, this article reviews the relationship between NF-κB and renal resident cells and their role in the pathogenesis of LN, with an aim to gain a deeper understanding of the underlying cellular and molecular mechanisms involved in LN and provide theoretical references for application in LN prevention and treatment.

Key words: Lupus nephritis, NF-κB pathway, Renal resident cells, Mechanism of action

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