Mitochondria in lung biology and pathology: more than just a powerhouse

被引:155
作者
Schumacker, Paul T. [1 ]
Gillespie, Mark N. [2 ]
Nakahira, Kiichi [3 ]
Choi, Augustine M. K. [3 ]
Crouser, Elliott D. [4 ]
Piantadosi, Claude A. [5 ]
Bhattacharya, Jahar [6 ]
机构
[1] Northwestern Univ, Feinberg Sch Med, Dept Pediat, Chicago, IL 60611 USA
[2] Univ S Alabama, Coll Med, Dept Pharmacol, Mobile, AL 36688 USA
[3] Weill Cornell Med Coll, Dept Med, New York, NY USA
[4] Ohio State Univ, Coll Med, Dept Internal Med, Columbus, OH 43210 USA
[5] Duke Univ, Sch Med, Dept Med, Durham, NC 27706 USA
[6] Columbia Univ, Med Ctr, Dept Physiol & Cellular Biophys, New York, NY USA
基金
美国国家卫生研究院;
关键词
hypoxia; lung injury; mitochondrial biogenesis; mitochondrial transfer; mtDNA; HYPOXIC PULMONARY VASOCONSTRICTION; INDUCED MTDNA DAMAGE; GATED K+ CHANNELS; DNA DAMAGE; SMOOTH-MUSCLE; OXIDATIVE STRESS; COMPLEX-III; TRANSCRIPTION FACTOR; MAMMALIAN-CELLS; TARGET GENES;
D O I
10.1152/ajplung.00073.2014
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
An explosion of new information about mitochondria reveals that their importance extends well beyond their time-honored function as the "powerhouse of the cell." In this Perspectives article, we summarize new evidence showing that mitochondria are at the center of a reactive oxygen species (ROS)-dependent pathway governing the response to hypoxia and to mitochondrial quality control. The potential role of the mitochondrial genome as a sentinel molecule governing cytotoxic responses of lung cells to ROS stress also is highlighted. Additional attention is devoted to the fate of damaged mitochondrial DNA relative to its involvement as a damage-associated molecular pattern driving adverse lung and systemic cell responses in severe illness or trauma. Finally, emerging strategies for replenishing normal populations of mitochondria after damage, either through promotion of mitochondrial biogenesis or via mitochondrial transfer, are discussed.
引用
收藏
页码:L962 / L974
页数:13
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