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According to studies, islet vascular fibrosis may play an important role in the progression of type 2 diabetes, but no mouse model has yet been able to conduct detailed mechanism studies to understand how dysfunctional islet microvascular vessels play a role in the pathogenesis of diabetes.
here, researchers reported that genetically modified AktTg mice, unlike other mice, showed increased deposition of extracellular substrate (ECM) proteins in the area around blood vessels, allowing researchers to study the cellular mechanisms that cause islet vascular fibrosis.
using immunoglostification, the researchers tagged islet microvascular systems and ECMs on pancreatic slices in AktTg mice and human donors, and performed genealogy tracking to track the fate of islet cells.
researchers compared islet microvascular reactions in live pancreatic slices in wild and AktTg mice.
in the AktTg mouse model, the researchers found that vascular cells proliferated widely, transforming them into fibrosis-promoting fibroblasts and largely promoting vascular fibrosis.
Increased deposition of type I collagen, fibrotin and peritonal myoprotein in the islet waslet islet isin isin and impaired capillary response caused by epinephrine (epinephrine) and high sugar in live pancreatic slices.
, the researchers' study illustrates how AktTg mice shed light on the cellular mechanisms of the development of islet vascular fibrosis, in which changes in the ideosis of weekly cells lead to vascular dysfunction.
because AktTg mice β more cells and secrete more insulin.
in a future study, researchers will test β cell secretion products to determine the role and other surrounding weekly cell esograms reside in the microenn environment under islet physiological and pathophysiological conditions.
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