-7

Sanjoy K Chowdhury1, Wei Liu1, Min Zi1

  • 1From Faculty of Biology, Medicine and Health (S.K.C., W.L., M.Z., Y.L., S.W., H.T., S.P., C.B.M., M.R.B., E.J.C., H.A.S., X.W.) and School of Physics and Astronomy (S.C., H.Z.), University of Manchester, United Kingdom; Atherosclerosis Research Centre, Nanjing Medical University, Jiangsu, China (Y.J.); Institute of Molecular Medicine, Peking University, Beijing, China (X.Z., R.X.); Case Cardiovascular Research Institute, Case Western Reserve University, Cleveland, OH (R.Z., X.L., M.K.J.); Department of Pharmacology, University of Oxford, United Kingdom (M.L.); and Department of Cardiology and Pneumology, University Medical Center Göttingen, Germany (L.C., K.G.).

Circulation
|December 1, 2016
PubMed
まとめ

ミトゲン活性化キナーゼキナーゼ7欠乏症は,カリウムチャネル遺伝子発現を阻害することによって,心房不律のリスクを高めます. この経路をバルプロ酸で標的にすることで,新しい抗不律性療法が提供される可能性があります.

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