心脏TRPM7导致射血分数保留的糖尿病性心力衰竭。
Cardiac TRPM7 Causes Diabetic Heart Failure With Preserved Ejection Fraction.
作者信息
Liu Man, Liu Hong, Kang Gyeoung-Jin, Hartweck Lynn M, Feng Feng, Kim Eunji, Prins Kurt W, Dudley Samuel C
机构信息
Cardiovascular Division, Department of Medicine, Lillehei Heart Institute, University of Minnesota-Twin Cities, Minneapolis, Minnesota, USA.
Cardiovascular Division, Department of Medicine, Lillehei Heart Institute, University of Minnesota-Twin Cities, Minneapolis, Minnesota, USA.
出版信息
JACC Basic Transl Sci. 2025 Aug;10(8):101321. doi: 10.1016/j.jacbts.2025.101321.
Hypomagnesemia (HypoMg) and subsequent oxidative stress cause diabetic cardiac diastolic dysfunction and heart failure with preserved ejection fraction. A Mg transporter with channel and kinase function, transient receptor potential cation channel subfamily M 7 (TRPM7), is upregulated in HypoMg. Diabetes mellitus mice had HypoMg and elevated TRPM7 expression in the heart. TRPM7 kinase mediated mitochondrial dysfunction and cardiac diastolic dysfunction in HypoMg. TRPM7 kinase enhanced mitochondrial Fgr expression, with subsequent complex II dysfunction and mitochondrial reactive oxygen species overproduction. Inhibition of TRPM7 kinase represents a potential novel therapeutic strategy to treat diabetic heart failure with preserved ejection fraction.
低镁血症（低镁）及随后的氧化应激会导致糖尿病性心脏舒张功能障碍和射血分数保留的心力衰竭。一种具有通道和激酶功能的镁转运体，瞬时受体电位阳离子通道亚家族M 7（TRPM7），在低镁血症中上调。糖尿病小鼠存在低镁血症且心脏中TRPM7表达升高。TRPM7激酶介导低镁血症中的线粒体功能障碍和心脏舒张功能障碍。TRPM7激酶增强线粒体Fgr表达，随后导致复合物II功能障碍和线粒体活性氧过度产生。抑制TRPM7激酶代表了一种治疗射血分数保留的糖尿病心力衰竭的潜在新治疗策略。
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