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Autophagy is the name given to a collection of cellular maintenance processes that recycle damaged structures, unwanted protein, and other metabolic waste. Many forms of stress, such as heat, lack of nutrients, and so forth spur greater autophagy, and this is thought to be a large part of why mild, temporary stress can produce lasting benefits to health – a process known as hormesis. Cell function is improved, and thus tissue function is improved. Many of the methods shown to modestly slow aging in laboratory species involve increased autophagy, and at least some, such as the practice of calorie restriction, have been shown to depend on functional autophagy for their benefits.
Rather than applying stress to generate autophagy, development programs focus on the use of small molecule drugs to influence the gene networks that regulate stress responses – such as targeting mTOR through rapamycin and analogous mTOR inhibitors. The research results here are an example of the type, showing that forcing a greater pace of autophagy helps to resist some of the metabolic consequences of type 2 diabetes – though of course this compares unfavorably with low calorie diets and consequent reduction in excess visceral fat tissue, the cause of the condition, as an approach to therapy in this specific case.
Vascular dysfunction is a major complication in type 2 diabetes (T2D). It has been suggested dysregulation of autophagy is associated with various cardiovascular diseases. However, the relationship between autophagy and vascular dysfunction in T2D remains unclear. Thus, we examined whether reduced autophagy is involved in vascular dysfunction and stimulation of autophagy could improve vascular function in diabetes.
Ten to 12-week old male type 2 diabetic (db-/db-) mice and their control (db-/db+) mice were treated with rapamycin or trehalose. Mesenteric arteries (MAs) were mounted in the arteriography and diameter was measured. Western blot analysis and immunofluorescence staining were assessed. Myogenic response (MR) was significantly increased, whereas endothelium-dependent relaxation (EDR) was significantly attenuated in the MAs of diabetic mice. These results were associated with increased expressions of LC3II, p62, and beclin-1 in diabetic mice.
Treatment of autophagy stimulators significantly reduced the potentiation of MR and improved EDR in the diabetic mice. Furthermore, autophagy stimulation normalized expressions of LC3II, p62, and beclin-1 in the diabetic mice. In addition, phosphorylation level of eNOS was decreased in diabetic mice, which was restored by rapamycin and trehalose. In conclusion, T2D impairs vascular function by dysregulated autophagy. Therefore, autophagy could be a potential target for overcoming diabetic microvascular complications.