Division of Nephrology-Hypertension and O'Brien Kidney Center, Center for Renal Translational Medicine, Stein Institute for Research on Aging, University of California San Diego and the Veterans Administration San Diego Healthcare System, La Jolla, CA, USA.
Nephrol Dial Transplant. 2013 Nov;28 Suppl 4(Suppl 4):iv29-36. doi: 10.1093/ndt/gft229. Epub 2013 Jul 30.
Obesity is a long-term source of cellular stress that predisposes to chronic kidney disease (CKD). Autophagy is a homeostatic mechanism for cellular quality control through the disposal and recycling of cellular components. During times of cellular stress, autophagy affords mechanisms to manage stress by selectively ridding the cell of the accumulation of potentially toxic proteins, lipids and organelles. The adaptive processes employed may vary between cell types and selectively adjust to the insult by inducing components of the basic autophagy machinery utilized by the cells while not under duress. In this review, we will discuss the autophagic responses of organs to cellular stressors, such as high-fat diet, obesity and diabetes, and how these mechanisms may prevent or promote the progression of disease. The identification of early cellular mechanisms in the advent of obesity- and diabetes-related renal complications could afford avenues for future therapeutic interventions.
肥胖是导致慢性肾脏病（CKD）的长期细胞应激源。自噬是一种通过处理和回收细胞成分来实现细胞质量控制的稳态机制。在细胞应激时，自噬通过选择性地清除潜在有毒蛋白质、脂质和细胞器，为细胞提供了应对压力的机制。所采用的适应性过程可能因细胞类型而异，并通过诱导细胞在不受压力时使用的基本自噬机制的成分来选择性地调整以应对损伤。在这篇综述中，我们将讨论器官对细胞应激源（如高脂肪饮食、肥胖和糖尿病）的自噬反应，以及这些机制如何预防或促进疾病的进展。在肥胖和糖尿病相关的肾脏并发症出现时，识别早期细胞机制可能为未来的治疗干预提供途径。
