Fig. 6: Diabetic microenvironment and aberrant activation of Notch-1 signaling affect podocyte restoration after islet transplantation by regulating the balance between autophagy and apoptosis. | Cell Death & Disease

Fig. 6: Diabetic microenvironment and aberrant activation of Notch-1 signaling affect podocyte restoration after islet transplantation by regulating the balance between autophagy and apoptosis.

From: Aberrant activation of Notch-1 signaling inhibits podocyte restoration after islet transplantation in a rat model of diabetic nephropathy

Fig. 6: Diabetic microenvironment and aberrant activation of Notch-1 signaling affect podocyte restoration after islet transplantation by regulating the balance between autophagy and apoptosis.The alternative text for this image may have been generated using AI.

Islet transplantation has demonstrated its significant effects on renal damage and podocyte injury. However, in the microenvironment of diabetic nephropathy, many factors can induce podocyte injury. Notch-1 signaling can be activated by many factors, such as high-glucose stress, mechanical damages, hemodynamic changes, and oxidative stress reaction. Highly activated status of Notch-1 intracellular domain (NICD) can translocate into the nucleus and upregulate the expressions of Hes/Hey transcription factors and VEGF, which ultimately lead to podocyte apoptosis. The balance between autophagy and apoptosis of podocyte is also critical during the process of treatment of glomerular diseases and podocyte restoration. Inhibiting γ-secretase by DAPT can decrease podocyte apoptosis to some extent under the condition of DN, but it cannot upregulate the level of autophagy expression of podocytes. Therefore, the microenvironment should be taken into consideration during clinical therapies on diabetic patients through islet transplantation

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