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Annu Rev Physiol. 2017 Feb 10;79:495-515. doi: 10.1146/annurev-physiol-022516-034322. Epub 2016 Dec 7.

Mitochondrial Dysfunction in Lung Pathogenesis.

Author information

1
Departments of Medicine, Pathology, and Anesthesiology, Duke University Medical Center, Durham, North Carolina 27710; email: Piant001@mc.duke.edu.
2
Departments of Anesthesiology and Pathology, Duke University School of Medicine, Durham, North Carolina 27710; email: Hagir.Suliman@duke.edu.

Abstract

Remarkable new roles for mitochondria in calcium handling, apoptosis, heme turnover, inflammation, and oxygen and nutrient sensing have been discovered for organelles that were once thought to be simple energy converters. Although deficits in mitochondrial function are often associated with energy failure and apoptosis, working cells maintain a mitochondrial reserve that affords the organelles distinct homeostatic sensing and regulatory abilities in lung cells. As primary intracellular sources of oxidants, mitochondria serve as critical monitors and modulators of vital oxidation-reduction processes, including mitochondrial biogenesis, mitophagy, inflammasome activation, cell proliferation, and prevention of fibrosis. These processes participate in disease pathogenesis in all lung regions mainly when interference with mitochondrial quality control mechanisms impedes their roles in maintenance of lung health. Sharper identification of mitochondrial-driven signaling mechanisms in specific lung cell types will better refine our understanding of respiratory disease pathogenesis and lead to new diagnostic and therapeutic measures to support mitochondrial quality.

KEYWORDS:

inflammasome; mitochondrial biogenesis; mitophagy; oxidants; reactive oxygen species; respiration

[Indexed for MEDLINE]

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