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Islet pericytes convert into profibrotic myofibroblasts in a mouse model of islet vascular fibrosis – published online 18/05/2020

Luciana Mateus Gonçalves, Elizabeth Pereira, João Pedro Werneck de Castro, Ernesto Bernal-Mizrachi, Joana Almaça

Vascular fibrosis is a very common lesion in islets from individuals with type 2 diabetes but its aetiology has not yet been determined. Until now, mouse models that enable us to study the role of dysfunctional islet microvasculature in diabetes pathogenesis have not been available. In this issue, Mateus Gonçalves et al (https://doi.org/10.1007/s00125-020-05168-7) report that a transgenic mouse model of beta cell expansion (the AktTg mouse) exhibits an increased deposition of extracellular matrix proteins around islet blood vessels, allowing for the study of cellular mechanisms that lead to islet vascular fibrosis and its functional consequences. They found that islet pericytes proliferated extensively in this model and were converted into profibrotic myofibroblasts. Vascular alterations were associated with diminished islet blood perfusion and impaired islet vascular responses to noradrenaline and glucose, which led to a decrease in glucose-stimulated insulin secretion per beta cell unit in these transgenic mice. The authors conclude that the AktTg mouse model can now be used to conduct studies aimed at elucidating the role of insulin or other beta cell secretory products in determining the number, phenotype and function of islet pericytes. They state that elucidating the crosstalk between pericytes and beta cells is necessary to fully understand the pathogenesis of islet adaptation in diabetes.

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