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肾小球疾病中的炎症

Inflammation in glomerular diseases.

作者信息

Xiong Yongqing, Li Wei, Jin Songzhi, Wan Shujing, Wu Suzhen

机构信息

School of Rehabilitation Medicine, Gannan Medical University, Ganzhou, China.

School of Basic Medicine, Gannan Medical University, Ganzhou, China.

出版信息

Front Immunol. 2025 Mar 4;16:1526285. doi: 10.3389/fimmu.2025.1526285. eCollection 2025.


DOI:10.3389/fimmu.2025.1526285
PMID:40103820
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11913671/
Abstract

The structural and functional integrity of glomerular cells is critical for maintaining normal kidney function. Glomerular diseases, which involve chronic histological damage to the kidney, are related to injury to glomerular cells such as endothelial cells, mesangial cells (MCs), and podocytes. When faced with pathogenic conditions, these cells release pro-inflammatory cytokines such as chemokines, inflammatory factors, and adhesion factors. These substances interact with glomerular cells through specific inflammatory pathways, resulting in damage to the structure and function of the glomeruli, ultimately causing glomerular disease. Although the role of inflammation in chronic kidney diseases is well known, the specific molecular pathways that result in glomerular diseases remain largely unclear. For a long time, it has been believed that only immune cells can secrete inflammatory factors. Therefore, targeted therapies against immune cells were considered the first choice for treating inflammation in glomerular disease. However, emerging research indicates that non-immune cells such as glomerular endothelial cells, MCs, and podocytes can also play a role in renal inflammation by releasing inflammatory factors. Similarly, targeted therapies against glomerular cells should be considered. This review aims to uncover glomerular diseases related to inflammation and pathways in glomerular inflammation, and for the first time summarized that non-immune cells in the glomerulus can participate in glomerular inflammatory damage by secreting inflammatory factors, providing valuable references for future strategies to prevent and treat glomerular diseases. More importantly, we emphasized targeted glomerular cell therapy, which may be a key direction for the future treatment of glomerular diseases.

摘要

肾小球细胞的结构和功能完整性对于维持正常肾功能至关重要。肾小球疾病涉及肾脏的慢性组织学损伤,与内皮细胞、系膜细胞(MCs)和足细胞等肾小球细胞的损伤有关。当面临致病条件时,这些细胞会释放促炎细胞因子,如趋化因子、炎症因子和黏附因子。这些物质通过特定的炎症途径与肾小球细胞相互作用,导致肾小球结构和功能受损,最终引发肾小球疾病。尽管炎症在慢性肾脏病中的作用已为人所知,但导致肾小球疾病的具体分子途径在很大程度上仍不清楚。长期以来,人们一直认为只有免疫细胞能分泌炎症因子。因此,针对免疫细胞的靶向治疗被认为是治疗肾小球疾病炎症的首选。然而,新出现的研究表明,肾小球内皮细胞、MCs和足细胞等非免疫细胞也可通过释放炎症因子在肾脏炎症中发挥作用。同样,也应考虑针对肾小球细胞的靶向治疗。本综述旨在揭示与炎症相关的肾小球疾病以及肾小球炎症中的途径,并首次总结了肾小球中的非免疫细胞可通过分泌炎症因子参与肾小球炎症损伤,为未来预防和治疗肾小球疾病的策略提供有价值的参考。更重要的是,我们强调了靶向肾小球细胞治疗,这可能是未来治疗肾小球疾病的关键方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3af9/11913671/3ad63bded485/fimmu-16-1526285-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3af9/11913671/f5584ee8513b/fimmu-16-1526285-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3af9/11913671/3ad63bded485/fimmu-16-1526285-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3af9/11913671/f5584ee8513b/fimmu-16-1526285-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3af9/11913671/3ad63bded485/fimmu-16-1526285-g002.jpg

相似文献

[1]
Inflammation in glomerular diseases.

Front Immunol. 2025-3-4

[2]
Fn14 in podocytes and proteinuric kidney disease.

Biochim Biophys Acta. 2013-12

[3]
The glomerulus--a view from the inside--the endothelial cell.

Int J Biochem Cell Biol. 2010-6-9

[4]
Unraveling the epigenetic landscape of glomerular cells in kidney disease.

J Mol Med (Berl). 2021-6

[5]
Role of the Innate Immune Response in Glomerular Disease Pathogenesis: Focus on Podocytes.

Cells. 2024-7-6

[6]
L22. Crescent formation: unraveling local mediators that break glomerular epithelial cell tolerance to immune injury.

Presse Med. 2013-4

[7]
Expression of CCN1 (CYR61) in developing, normal, and diseased human kidney.

Am J Physiol Renal Physiol. 2007-10

[8]
Differential expression of functional Fc-receptors and additional immune complex receptors on mouse kidney cells.

Mol Immunol. 2013-8-1

[9]
The Players: Cells Involved in Glomerular Disease.

Clin J Am Soc Nephrol. 2016-9-7

[10]
Crosstalk in glomerular injury and repair.

Curr Opin Nephrol Hypertens. 2015-5

本文引用的文献

[1]
Roles of macrophages in lupus nephritis.

Front Pharmacol. 2024-11-14

[2]
Potential biomarkers of recurrent FSGS: a review.

BMC Nephrol. 2024-8-12

[3]
Novel Biomarkers for the diagnosis of diabetic nephropathy.

Caspian J Intern Med. 2024

[4]
Mitochondrial metabolic reprogramming in diabetic kidney disease.

Cell Death Dis. 2024-6-24

[5]
Normal and Dysregulated Sphingolipid Metabolism: Contributions to Podocyte Injury and Beyond.

Cells. 2024-5-22

[6]
Podocyte-targeted therapies - progress and future directions.

Nat Rev Nephrol. 2024-10

[7]
JAK2 inhibitors improve RA combined with pulmonary fibrosis in rats by downregulating SMAD3 phosphorylation.

Int J Rheum Dis. 2024-5

[8]
Clinical significance of urinary inflammatory biomarkers in patients with IgA nephropathy.

BMC Nephrol. 2024-4-22

[9]
Crosstalk among podocytes, glomerular endothelial cells and mesangial cells in diabetic kidney disease: an updated review.

Cell Commun Signal. 2024-2-19

[10]
Cytoskeleton Rearrangement in Podocytopathies: An Update.

Int J Mol Sci. 2024-1-4

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