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News highlights in June 2010
Autophagy hits heart
Autophagy is acutely upregulated to provide necessary nutrients during starvation for survival. Under normal condition, constitutive autophagy is critical to perform house-keeping functions to eliminate damaged organelles and dysfunctional long-lived proteins.
Ageing is associated with accumulation of dysfunctional proteins in cells. Autophagic activity is decreasing along with ageing. Studies in worms and flies show that reconstitution of autophagy can increase life span. A recent report by Taneike and colleagues explored the role of autophagy in age-related cardiomyopathy. In heart, autophagic activity is decreasing when ageing. Taneike et al eliminated autophagy in heart by knocking out an essential gene, ATG5, specifically in heart. The researchers found deteriorated cardiac function at 10 months of age in the deficient animals compared to wild type controls. The dysfunction of autophagy causes accumulation of dysfunctional mitochondrial, reduced mitochondrial efficiency and significant oxidative damage in cardiomyocytes. More interestingly, evidence of mitochondrial damage is obvious as early as 3 months old, before cardiac remodeling and dysfunction manifest. This study points to a possibility that autophagy is critical in maintaining cardiomyocyte homeostasis and autophagy may be a target for future therapeutic design for heart failure.Reference: Taneike M et al, Autophagy , June 2010.
Autophagy hits liver
Obesity is a condition of over-nutrient with various organs exposed to energy surplus. Obesity is associated with numerous metabolic dysfunctions and diseases. Liver, as the major organ to uptake and process nutrients, plays inevitable roles in maintenance of whole body energy homeostasis. In obesity, insulin signaling in liver is severely impaired and, over time, the important functions of liver, including lipogenesis and gluconeogenesis, are disrupted.
Autophagy is an evolutionarily conserved catabolic process. Autophagy can self-digest to provide necessary nutrients during starvation. Under normal conditions, autophagy is involved in maintenance of cellular homeostasis by clearing dysfunctional organelles and large protein aggregates. The association between autophagy and obesity has been implicated in several aspects recently. A new study from Yang and colleagues provided evidence suggesting impairment of autophagy in liver causes insulin resistance during obesity. Yang et al found autophagy is decreased in obese livers. This decline of autophagic activity is associated with blunting of insulin signaling. In autophagy-deficient cells, Yang et al showed that the insulin stimulated downstream targets cannot be activated. Acute inactivation of autophagy using ShRNA in liver causes insulin resistance in wild type animals while reconstitution of autophagy in obese mice can restore insulin sensitivity. The study by Yang and colleagues provides a new link between obesity and autophagy and may shed new light on the mechanism of insulin resistance in obesity. This study is landed in Cell Metabolism.Reference: Yang L et al, Cell Metab , June 2010.
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