A role of dysregulated glycosylation of hypoxia-inducible factors in the pathogenesis of cardio-renal syndrome

本研究旨在从缺氧诱导的转录因子糖基化失调的角度，深入了解心肾综合征发病的分子机制。甲基乙二醛（MG）是一种高活性代谢物，已知可在慢性肾脏疾病中积累。在细胞培养实验中，MG对缺氧反应没有影响。另一方面，高葡萄糖抑制细胞缺氧反应约20%。本研究结果为了解心肾综合征和代谢综合征的分子机制提供了线索。

This study was designed to gain insight into molecular mechanisms in the pathogenesis of the cardio-renal syndrome, from a viewpoint of dysregulated glycosylation of hypoxia-inducible transcription factors. Methylglyoxal (MG) is a highly reactive metabolite and is known to accumulate in chronic kidney disease. In cell culture experiments, MG failed to impact hypoxia response. On the other hand, high glucose dampened cellular hypoxia response by approximately 20%. Results of the present study provide a clue to understanding molecular mechanisms underlying the cardio-renal syndrome as well as the metabolic syndrome.