نبذة مختصرة : There is mounting evidence that the circadian system is integral to the development and management of diabetic complications. Circadian disruption increases the risk of diabetes, which, in turn, causes desynchrony in the circadian system and molecular clock that exists in the cell. Despite several of the underlying pathologies being either controlled by or linked to the circadian clock, little is known about the impact of a dysfunctional circadian system in the most common complication of diabetes, diabetic retinopathy (DR). For example, hypoxia, a major therapeutic target for diabetic retinopathy, alters the expression of the core genes in the molecular clock in endothelial cells. This presents a novel mechanistic hypothesis for the role of a disrupted circadian clock in diabetic retinopathy.
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