The Role of Podocytes in Lupus Pathology

Overview

Journal Curr Rheumatol Rep

Publisher Current Science

Specialty Rheumatology

Date 2024 Dec 28

PMID 39731699

Authors

Kayaho Maeda

Reza Abdi

George C Tsokos

Affiliations

Soon will be listed here.

Abstract

Purpose Of Review: Kidney injury due to lupus nephritis (LN) is a severe and sometimes life-threatening sequela of systemic lupus erythematosus. Autoimmune injury to podocytes has been increasingly demonstrated to be a key driver of LN-related kidney injury because these cells play key roles in glomerular filtration barrier homeostasis. Irreparable podocyte injury impairs these processes and can lead to proteinuria, which is an indicator of poor prognosis in LN. This review highlights recent advances in our understanding of the involvement of podocytes in the pathogenesis of LN and discusses new podocyte-targeted therapeutic strategies.

Recent Findings: Podocytes play a key role in glomerular filtration barrier homeostasis, both by helping to secrete and organize the glomerular basement membrane and by the formation of a glomerular slit diaphragm between adjacent cells. Recent studies revealed the involvement of abnormal calcium signaling, dysregulation of actin-related proteins, and mitotic catastrophe in LN progression. In addition, podocytes express many molecules related to the innate and adaptive immune responses. IgG from patients with LN induces direct injury of podocytes, inflammasome, and interactions with immune cells which have been shown to promote the development of LN. Our understanding of the role of podocytes in the pathogenesis of LN has been improved. Recent studies have shed light on potential therapeutic strategies targeting podocytes to control kidney injury.

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