Review highlights mitochondrial dysfunction's role in lung diseases like COPD and asthma, suggesting therapeutic implications.
Mitochondrial structural and functional alterations have been linked to patho-genesis and disease progression across a spectrum of chronic and acute lung diseases. With substantial and diverse energy requirements, the metabolically active lungs sup-port essential functions such as gas exchange, mucociliary clearance, and immune de-fense. This review focuses on the critical role of mitochondrial mechanisms and their subsequent dysfunction in the pathogenesis and progression of several debilitating lung pathologies. Specifically, we will explore how changes in mitochondrial dynamics (fusion and fission), bioenergetics, quality control mechanisms such as mitophagy, and the production of reactive oxygen species (ROS) contribute to the cellular and molecu-lar foundations of various lung diseases. These pathologies include asthma, which is often manageable; COPD and idiopathic pulmonary fibrosis (IPF), which cause pro-gressive decline; and acute respiratory distress syndrome (ARDS) and lung cancer, which can be immediately life-threatening. This review highlights the growing under-standing of mitochondrial dysfunction as a central factor in the development and pro-gression of lung diseases. It focuses on how disruptions in mitochondrial homeostasis contribute to disease pathogenesis and the potential implications of mitochon-dria-targeted therapeutic approaches to improve patient outcomes.
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Broschek et al. (2025) studied this question.
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