Mitochondria are dynamic organelles, which couple the various cellular processes that regulate metabolism, cell proliferation and survival. Environmental stress can cause mitochondrial dysfunction and dynamic changes including reduced mitochondrial biogenesis, oxidative phosphorylation and ATP production, as well as mitophagy impairment, which leads to increased ROS, inflammatory responses and cellular senescence. Oxidative stress, inflammation and cellular senescence all have important roles in the pathogenesis of chronic lung diseases, such as chronic obstructive pulmonary disease, pulmonary fibrosis and bronchopulmonary dysplasia. In this review, we discuss the current state on how mitochondrial dysfunction affects inflammatory responses and cellular senescence, the mechanisms of mitochondrial dysfunction underlying the pathogenesis of chronic lung diseases and the potential of mitochondrial transfer and replacement as treatments for these diseases.
AbbreviationsAMPK, AMP-activated protein kinase; α-SMA, α-smooth muscle actin; BPD, bronchopulmonary dysplasia; COPD, chronic obstructive pulmonary disease; DRP1, DNM1L, dynamin 1-like; Δψm, mitochondrial membrane potential; ETC, electron transport chain; FIS1, fission 1; MDVs, mitochondria-derived vesicles; Mfn, mitofusin; MiDAS, mitochondrial dysfunctionassociated senescence; MPTP, mitochondrial permeability transition pore; mtDNA, mitochondrial DNA; mtROS, mitochondrial ROS; O 2 .À , superoxide anion; OPA1, optic atrophy 1; PINK1, PTEN-induced putative kinase 1; SASP, senescenceassociated secretory phenotype; UCP, mitochondrial uncoupling protein