Abstract
Lung diseases such as chronic obstructive pulmonary disease, asthma, pulmonary arterial hypertension, or idiopathic pulmonary fibrosis are major causes of morbidity and mortality. Complex, their physiopathology is multifactorial and includes lung mitochondrial dysfunction and enhanced reactive oxygen species (ROS) release, which deserves increased attention. Further, and importantly, circulating blood cells (peripheral blood mononuclear cells-(PBMCs) and platelets) likely participate in these systemic diseases. This review presents the data published so far and shows that circulating blood cells mitochondrial oxidative capacity are likely to be reduced in chronic obstructive pulmonary disease (COPD), but enhanced in asthma and pulmonary arterial hypertension in a context of increased oxidative stress. Besides such PBMCs or platelets bioenergetics modifications, mitochondrial DNA (mtDNA) changes have also been observed in patients. These new insights open exciting challenges to determine their role as biomarkers or potential guide to a new therapeutic approach in lung diseases.
Highlights
Lung diseases, especially chronic obstructive pulmonary disease (COPD), asthma, pulmonary arterial hypertension (PAH), and/or idiopathic pulmonary fibrosis (IPF) are main causes of mortality, resulting in significant health and economic burdens worldwide
Wiegman et al showed an association between mitochondrial dysfunction and excessive mtROS levels in airway smooth muscle cells from COPD patients, which contributes to enhanced inflammation and cell proliferation [31]
Mitochondrial dysfunction associated with lung inflammation and oxidative stress contributes to COPD, asthma, PAH, and idiopathic pulmonary fibrosis
Summary
Especially chronic obstructive pulmonary disease (COPD), asthma, pulmonary arterial hypertension (PAH), and/or idiopathic pulmonary fibrosis (IPF) are main causes of mortality, resulting in significant health and economic burdens worldwide. PAH or IPF are less common but are characterized by poor prognosis [3,4] Based on this evidence, it appears important to gain new insight into lung diseases pathophysiology and to analyze potential biomarkers to better reveal lung function, diagnose, and predict the prognosis of these diseases. As observed during cardiovascular diseases, mitochondrial dysfunctions deserve to be further studied, both at the local and at the circulating levels [5]. Mitochondrial abnormalities are involved in lung diseases but direct evidence of cJa. rCdliino. U20l2a0r, 9d,i1s2e5a3ses, mitochondrial dysfunctions deserve to be further studied, both at the l2oocfa2l0 and at the circulating levels [5]. Mitochondrial abnormalities are involved in lung diseases bmutitdoicrhecotnedvriidael ndcyesofufnmcittioocnhionnhdurimaladnysstfuudnicetsioins liinmhiutemda, nbesctauudsieesoifstlhime idteiffid,cbuelctyautsoeboifotphseydtiifsfsiucuesltyin tothbeisoepfsryaitlipssautieesnitns.these frail patients. Akntopwrenseanntd, tthheeloinbkjebcteitvweeoefnthPiBsMreCviseowr ipslatoteplertessemnittothcheodnadtaripalufbulinschteiodnsaonfdar luanndg dtoisdeaissceussiss tphoeoprloyteknntoiawlninatnerdestht eofosbtjuecdtyivinegofcitrhciuslraetviniegwblios otodpcreellssenmtitthoechdoantadrpiualbfliusnhcetdiosno afanrd ROS production during COPD, asthma, PAH, and IPF
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