Mitochondria as integrators of signal transduction and energy production in cardiac physiology and disease

被引:17
作者
Frohman, Michael A. [1 ,2 ]
机构
[1] SUNY Stony Brook, Ctr Mol Med 438, Stony Brook, NY 11794 USA
[2] SUNY Stony Brook, Dept Pharmacol, Ctr Dev Genet, Stony Brook, NY 11794 USA
来源
JOURNAL OF MOLECULAR MEDICINE-JMM | 2010年 / 88卷 / 10期
关键词
Mitochondria; Fusion; Fission; ROS; Signaling; PULMONARY ARTERIAL-HYPERTENSION; FUSION; MITOFUSIN-2; APOPTOSIS; DYNAMICS; PATHWAY; FISSION; BIOLOGY; MUSCLE; RATS;
D O I
10.1007/s00109-010-0662-x
中图分类号
Q3 [遗传学];
学科分类号
071007 [遗传学];
摘要
Fascinating links are beginning to be discovered between mitochondrial function and cardiac physiology and disease in the context of diverse signaling mechanisms, energy production, and intersection with pathways producing reactive oxygen species. Proteins long known to drive mitochondrial fusion and fission are now reported to have emergent functions in intracellular calcium homeostasis, apoptosis, and vascular smooth muscle cell proliferation, all key issues in cardiac disease. Moreover, mitochondrial fusion has been demonstrated to be required for normal myofibril organization in skeletal muscle, and decreasing fission may confer protection against ischemic heart disease. These processes broaden the traditional role in energy production undertaken by mitochondria and provide new directions for potential therapeutic leads.
引用
收藏
页码:967 / 970
页数:4
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