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Updated: Sep 13, 2025
Scaffold-supported Transplantation of Islets in the Epididymal Fat Pad of Diabetic Mice
Published on: July 23, 2017
March5-mediated Trim28 degradation preserves islet β-cell function in mice
Yangshan Chen1, Wei Pang1, Guixing Ma2
1Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Key University Laboratory of Metabolism and Health of Guangdong, Department of Biochemistry, SUSTech Homeostatic Medicine Institute, School of Medicine, Southern University of Science and Technology, Shenzhen, China.
Researchers found that March5 and Trim28 regulate beta-cell function. Modulating this pathway, involving Kindlin-2 and MafA, could restore insulin production and improve glucose tolerance in diabetes.
Area of Science:
- Endocrinology
- Molecular Biology
- Metabolic Diseases
Background:
- Beta-cell dysfunction is central to diabetes pathogenesis.
- Regulatory mechanisms governing beta-cell function are not fully understood.
Purpose of the Study:
- To identify key regulators of beta-cell function.
- To elucidate the molecular pathway involving March5 and Trim28 in diabetes.
Main Methods:
- Analysis of March5 and Trim28 expression in human and mouse islets.
- Investigating the effects of March5 and Trim28 manipulation in mouse models.
- Assessing glucose tolerance and insulin production.
- Utilizing islet transplantation in diabetic mice.
Main Results:
- March5 downregulation and Trim28 upregulation correlate with impaired glucose tolerance.
- March5 deficiency impairs insulin production; overexpression improves it.
- March5 inhibits Trim28, preventing Kindlin-2 degradation and increasing MafA/insulin expression.
- Targeting the March5/Trim28/Kindlin-2/MafA pathway ameliorates diabetes in mouse models.
Conclusions:
- The March5/Trim28/Kindlin-2/MafA axis is a critical regulator of beta-cell function.
- This pathway represents a potential therapeutic target for diabetes treatment.
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