TY - JOUR
T1 - Mitochondria in lung biology and pathology
T2 - More than just a powerhouse
AU - Schumacker, Paul T.
AU - Gillespie, Mark N.
AU - Nakahira, Kiichi
AU - Choi, Augustine M.K.
AU - Crouser, Elliott D.
AU - Piantadosi, Claude A.
AU - Bhattacharya, Jahar
PY - 2014/6/1
Y1 - 2014/6/1
N2 - 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.
AB - 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.
KW - Hypoxia
KW - Lung injury
KW - Mitochondrial biogenesis
KW - Mitochondrial transfer
KW - mtDNA
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U2 - 10.1152/ajplung.00073.2014
DO - 10.1152/ajplung.00073.2014
M3 - Article
C2 - 24748601
AN - SCOPUS:84901697863
VL - 306
SP - L962-L974
JO - American Journal of Physiology - Lung Cellular and Molecular Physiology
JF - American Journal of Physiology - Lung Cellular and Molecular Physiology
SN - 1040-0605
IS - 11
ER -