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Lipotoxicity-induced circGlis3 impairs beta cell function and is transmitted by exosomes to promote islet endothelial cell dysfunction – published online 09/11/2021

Xiong graphical abstract

Li Xiong, Li Chen, Liting Wu, Weiman He, Dubo Chen, Zishan Peng, Jin Li, Xiaonan Zhu, Lei Su, Yanbing Li, Yingying Gong, Haipeng Xiao

Circular RNAs (circRNAs) play important roles in regulating beta cell function, and exosomes are essential mediators of intercellular communication. However, the role of exosomal circRNAs in type 2 diabetes is poorly understood. In this issue, Xiong et al ( report that circGlis3 (Gli-similar 3) participates in the development of type 2 diabetes in two different ways. In a conventional way, circGlis3 exerts deleterious effects on beta cells by inhibiting cell survival and insulin secretion. In an unconventional way, by acting as a mediator of intercellular crosstalk, beta cell-derived exosomal circGlis3 promotes islet endothelial cell dysfunction through the glucocorticoid modulatory element-binding protein 1 (GMEB1)/ heat shock protein 27 (HSP27) signalling pathway. They also demonstrate that exosomal circGlis3 is upregulated by lipotoxicity and is found at higher levels in mouse models of diabetes and in the serum of participants with type 2 diabetes. The authors conclude that this study provides new insights into the pathogenesis of type 2 diabetes and suggests the significance of circGlis3 as a potential biomarker and therapeutic target for the disease.

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