Abstract
Mitochondria are essential organelles for cell metabolism, growth, and function. Mitochondria in lung cells have important roles in regulating surfactant production, mucociliary function, mucus secretion, senescence, immunologic defense, and regeneration. Disruption in mitochondrial physiology can be the central point in several pathophysiologic pathways of chronic lung diseases such as chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, and asthma. In this review, we summarize how mitochondria morphology, dynamics, redox signaling, mitophagy, and interaction with the endoplasmic reticulum are involved in chronic lung diseases and highlight strategies focused on mitochondrial therapy (mito-therapy) that could be tested as a potential therapeutic target for lung diseases.
Highlights
Mitochondria are organelles present in all eukaryotic organisms with the classic role of generating most of the cellular energy
BMSCs exerted protective effects on the alveolar epithelium, restoring the alveolar metabolism in an acute lung injury (ALI) model. These cells transferred mitochondria to epithelial cells via connexin-43 gap junctions, directly or through underlying mechanisms of nanotubes and microvesicles, increasing alveolar adenosine triphosphate (ATP) production and reducing the hallmarks of ALI induced by lipopolysaccharide [176]
Mitochondria-targeted therapy may be a new therapeutic for restoring cellular bioenergetics and function in several airway diseases
Summary
Mitochondria are organelles present in all eukaryotic organisms with the classic role of generating most of the cellular energy. Mitochondrial intracellular movement is directly linked to calcium signals, which at different concentrations can induce mitochondrial translocation or provide a mechanism to retain mitochondria at Ca2+ signaling sites, regulating local power supply [62, 63] This can be important for epithelial cells in chronic lung diseases, such as asthma and COPD, which have a high cell turnover rate and increased energy requirements [20]. The exposure of hASM cells to TNFa, a proinflammatory cytokine that mediates the inflammatory response in asthma, led to the activation of ER stress pathways, disrupted mitochondrial proximity to the ER, and decreased Mfn protein expression, impairing mitochondrial mobility [134, 135] This creates the possibility of a vicious cycle with reduced Mfn expression and altered mitochondrial function [125]. Considering the close relationship between mitochondria and the ER, and their significant contribution to inflammasome activation and chronic lung diseases, MAMs and NRLP3 may be a potential new therapeutic target
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