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Review
. 2024 Jan 4:14:1303076.
doi: 10.3389/fimmu.2023.1303076. eCollection 2023.

Role of MCP-1 as an inflammatory biomarker in nephropathy

Affiliations
Review

Role of MCP-1 as an inflammatory biomarker in nephropathy

Yanlong Liu et al. Front Immunol. .

Abstract

The Monocyte chemoattractant protein-1 (MCP-1), also referred to as chemokine ligand 2 (CCL2), belongs to the extensive chemokine family and serves as a crucial mediator of innate immunity and tissue inflammation. It has a notable impact on inflammatory conditions affecting the kidneys. Upon binding to its receptor, MCP-1 can induce lymphocytes and NK cells' homing, migration, activation, differentiation, and development while promoting monocytes' and macrophages' infiltration, thereby facilitating kidney disease-related inflammation. As a biomarker for kidney disease, MCP-1 has made notable advancements in primary kidney diseases such as crescentic glomerulonephritis, chronic glomerulonephritis, primary glomerulopathy, idiopathic proteinuria glomerulopathy, acute kidney injury; secondary kidney diseases like diabetic nephropathy and lupus nephritis; hereditary kidney diseases including autosomal dominant polycystic kidney disease and sickle cell kidney disease. MCP-1 not only predicts the occurrence, progression, prognosis of the disease but is also closely associated with the severity and stage of nephropathy. When renal tissue is stimulated or experiences significant damage, the expression of MCP-1 increases, demonstrating a direct correlation with the severity of renal injury.

Keywords: MCP-1; hereditary nephropathy; inflammatory markers; primary nephropathy; secondary nephropathy.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Role of MCP-1 as an inflammatory marker in nephropathy.

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The author(s) declare that no financial support was received for the research, authorship, and/or publication of this article.
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