This review summarizes the molecular basis of mitochondrial fatty acid oxidation (FAO) as a core energy metabolic pathway in pulmonary tissues. FAO is presented not only as a source of ATP for lung cells but also as a participant in essential physiological processes such as alveolar surfactant synthesis. The author outlines regulatory features of mitochondrial FAO and how modulation of these pathways can influence lung cell metabolism and function. Specific molecular details are described in the full text; the abstract indicates an emphasis on FAO regulation without reporting mechanistic data in the abstract itself.
The review examines the complex regulatory roles of mitochondrial FAO across chronic respiratory conditions. It explicitly names chronic obstructive pulmonary disease (COPD), asthma, and pulmonary fibrosis as disorders in which FAO-related metabolic reprogramming contributes to pathogenesis. The author frames metabolic shifts in FAO as part of disease biology, suggesting that altered fatty acid utilization and mitochondrial metabolism may influence disease onset, progression, or tissue remodeling. The abstract does not provide disease-specific mechanistic findings or quantitative results; it summarizes that FAO plays diverse and disease-context–dependent regulatory roles.
Acute respiratory conditions are also covered, with the review addressing acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). The review positions FAO within the broader context of metabolic reprogramming during acute lung injury, indicating that mitochondrial fatty acid handling may affect cellular responses in ALI/ARDS. The abstract notes inclusion of these syndromes but does not report clinical data or trial outcomes, and emphasizes that much evidence comes from preclinical models.
Beyond inflammatory and fibrotic lung diseases, the review considers the role of mitochondrial FAO in lung cancer and pulmonary arterial hypertension (PAH). In these conditions, metabolic reprogramming — including alterations in FAO — is discussed as part of disease biology. The abstract identifies these disease areas as targets of the review but does not include detailed mechanistic or translational conclusions in the abstract itself.
The review summarizes potential therapeutic strategies that target FAO. These include:
The abstract clarifies that these proposed interventions are largely supported by preclinical evidence from animal experiments and in vitro studies. It does not report specific agents, dosages, or clinical trial results in the abstract.
A recurrent point in the review is that most therapeutic and mechanistic findings summarized are derived from preclinical models. The author explicitly notes that while these findings offer a theoretical framework for targeting FAO in respiratory disease, the direct clinical translatability remains to be validated. In other words, efficacy and safety of FAO-targeted approaches in humans require further clinical research.
The review positions mitochondrial FAO as an important and understudied regulator of pulmonary metabolism with relevance across a spectrum of respiratory diseases. It highlights FAO's roles in energy supply and physiological processes such as surfactant synthesis, and compiles disease-specific discussions and therapeutic concepts. The paper concludes by offering a theoretical foundation for future studies and by stressing the need for clinical validation of FAO-targeted strategies. The authors declare no competing interests.
Note on source material
All statements above are drawn from the PubMed abstract and bibliographic metadata for the review by Shuna Wei (Int Immunopharmacol, 2026; PMID 42275921). The abstract reports scope, disease areas covered, and the emphasis on preclinical evidence but does not provide detailed experimental results, drug names, or clinical trial data; those details were not reported in the abstract and would require consultation of the full text.