Abstract

Autophagy is an evolutionally conserved homeostatic process involving consecutive cellular steps for degrading and recycling aged or injured cytoplasmic components. Ample studies have indicated that a key role for basal autophagy in the maintenance of cellular homeostasis and function. However, inadequate or excessive autophagy in pathological conditions results may contribute to the impaired organismal function including development of diabetes and diabetic complications. Diabetes mellitus is a serious multifactorial metabolic disease linked to the high risk of cardiovascular and other chronic noncommunicable diseases. Increased lipotoxicity, inflammation, and oxidative stress are considered to contribute to the metabolic abnormalities in diabetic complications. Recent findings have also suggested a pivotal role for dysregulated autophagy in diabetogenesis and diabetic organ complications. Nonetheless, molecular mechanisms of dysregulated autophagy in diabetes are rather complex and involve multiple signaling pathways cooperating at various levels. This chapter summarizes recent advances in the molecular mechanisms behind autophagic regulation in diabetes and diabetic complications. A thorough and in-depth understanding on the molecular mechanisms leading to autophagy dysregulation in diabetes should offer promises toward new therapies for diabetes and diabetic complications.

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