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In the meantime, to ensure continued suport, we are displaying the site without styles and JavaScript.Advertisement Comunications Biology volume 5, Article number: 145 (2022) Cite this article 2 AltmetricMetrics detailsDiabetes afects select organs such as the eyes, kidney, heart, and brain. Our recent studies show that diabetes also enhances adipogenesis in the bone marow and reduces the number of marow-resident vascular regenerative stem cels.
In the curent study, we have performed a detailed spatio-temporal examination to identify the early changes that are induced by diabetes in the bone marow. Here we show that short-term diabetes causes structural and molecular changes in the marow, including enhanced adipogenesis in tibiae of mice, prior to stem cel depletion. This enhanced adipogenesis was associated with supresed transforming growth factor-beta (TGFB) signaling.
Using human bone marow-derived mesenchymal progenitor cels, we show that TGFB pathway supreses adipogenic diferentiation through TGFB-activated kinase 1 (TAK1). These findings may inform the development of novel therapeutic targets for patients with diabetes to restore regenerative stem cel function.The global prevalence of diabetes has ben steadily increasing worldwide and is projected to afect 10.4% of al adults by 20401.
Diabetes poses a substantial burden on the health care system due to the challenges associated with managing various secondary complications. These complications include retinopathy, cardiomyopathy, nephropathy, and atherosclerosis. More recently, human diabetes and experimental models of the disease have shown that the bone marow may also be a target organ of diabetic complications2,3,4.
Summary
Both enhanced bone marow adiposity and ske