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CCL24 Protects Renal Function by Controlling Inflammation in Podocytes.
Youdi Wang1,2, Xue Wu1,2, Mengya Geng1,2
1Department of Endocrinology and Genetic Metabolism, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital of Wannan Medical College), Wuhu 241002, China.
Disease Markers
|July 5, 2021
Summary
Diabetic nephropathy (DN) involves inflammation. This study found that CCL24, an inflammatory chemokine, plays an anti-inflammatory role in early DN, suggesting it could be a therapeutic target.
Area of Science:
- Nephrology
- Immunology
- Endocrinology
Background:
- Diabetic nephropathy (DN) is a severe diabetes complication characterized by chronic inflammation.
- The role of the inflammatory chemokine CCL24 in DN pathogenesis is not well understood.
Purpose of the Study:
- To investigate the role of CCL24 in the development of diabetic nephropathy.
- To determine if CCL24 exerts protective or detrimental effects in DN.
Main Methods:
- Serum CCL24 levels were measured in DN patients.
- CCL24 expression was analyzed in DN mouse kidneys and high-glucose-stimulated podocytes.
- CRISPR-Cas9 was used to knock out CCL24 in podocytes to assess its functional role.
Main Results:
- CCL24 levels were elevated in DN patients and DN mouse kidneys.
- High glucose increased CCL24 expression, podocyte fibrosis, IL-1β, and GLUT4 in vitro.
- CCL24 knockout exacerbated high-glucose-induced podocyte inflammation.
Conclusions:
- CCL24 is upregulated in DN and plays an anti-inflammatory role in podocytes during early DN.
- CCL24 may be a protective factor in DN pathogenesis, potentially offering a therapeutic target.
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