ArticleRespiratory research2019
Accumulation of damaged mitochondria in alveolar macrophages with reduced OXPHOS related gene expression in IPF.
Article in Respiratory research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 55 citations in OpenAlex.
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Integrated Single-Cell and Bulk RNA Sequencing Identifies Macrophage Heterogeneity and Mitophagy-Related Biomarkers in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2026Article
- Targeting immunosenescence in lung diseases: mechanistic insights and clinical interventions.BMC medicine · 2026Review
- Article
- Decreased Complex I Activity in Blood lymphocytes Correlates with Idiopathic Pulmonary Fibrosis Severity.Biochemical genetics · 2026Article
- The impact of macrophage metabolism on idiopathic pulmonary fibrosis development and treatment prospectives.Frontiers in immunology · 2026Review
- The gene regulatory networks shaping macrophage plasticity and altered function in fibrosis.Frontiers in immunology · 2026Review
- Mitophagy in idiopathic pulmonary fibrosis: from molecular mechanisms to therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Mechanisms and markers of lung ageing in health and disease.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Targeting E3 ubiquitin ligases: a new frontier in idiopathic pulmonary fibrosis treatment.Frontiers in immunology · 2025Review
- Unpacking the anti-fibrotic arsenal: molecular mechanisms and therapeutic translation of MSC-derived exosomes in pulmonary fibrosis.Frontiers in immunology · 2025Review
- Regulation of the NLRP3 inflammasome by autophagy and mitophagy.Immunological reviews · 2025Review
- Establishment and validation of a prognostic model for idiopathic pulmonary fibrosis based on mitochondrial-related genes.Journal of thoracic disease · 2024Article
- Review
- Macrophage polarization and its impact on idiopathic pulmonary fibrosis.Frontiers in immunology · 2024Review
- Mitophagy-promoting agents and their ability to promote healthy-aging.Biochemical Society transactions · 2023Article
- Ketogenesis promotes tolerance to Pseudomonas aeruginosa pulmonary infection.Cell metabolism · 2023Article
- The Role of Mitochondrial Dysfunction in Idiopathic Pulmonary Fibrosis: New Perspectives for a Challenging Disease.Biology · 2023Review
- Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundImpaired mitochondria homeostasis and function are established hallmarks of aging and increasing evidence suggests a link with lung fibrosis. Mitochondria homeostasis may be also affected in alveolar macrophages (AMs) in idiopathic pulmonary fibrosis (IPF). In this study, we used bronchoalveolar lavage (BAL), a tool for both clinical and research purposes, and a rich source of AMs.
methodsBAL samples were examined from 52 patients with IPF and 19 healthy individuals. Measurements of mitochondria reactive oxygen species (mtROS), mitochondria morphology and related gene expression were performed. Additionally, autophagy and mitophagy levels were analysed.
resultsMitochondria in AMs from IPF patients had prominent morphological defects and impaired transcription paralleled to a significant reduction of mitochondria homeostasis regulators PINK1, PARK2 and NRF1. mtROS, was significantly higher in IPF and associated with reduced expression of mitochondria-encoded oxidative phosphorylation (OXPHOS) genes. Age and decline in lung function correlated with higher mtROS levels. Augmentation of damaged, oxidised mitochondria in IPF AMs however was not coupled to increased macroautophagy and mitophagy, central processes in the maintenance of healthy mitochondria levels.
conclusionOur results suggest a perturbation of mitochondria homeostasis in alveolar macrophages in IPF.
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