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Identifier 000426211
Title Mitophagy and oxidation status of mitochondria in Idiopathic Pulmonary Fibrosis (IPF) macrophages – a study in bronchoalveolar lavage fluid (BALF).
Alternative Title Μιτοφαγία και επίπεδα οξείδωσης των μιτοχονδρίων στα μακροφάγα των ασθενών με Ιδιοπαθή Πνευμονική Ίνωση (ΙΠΙ)- μία μελέτη σε βρογχοκυψελιδικό έκπλυμα
Author Βασαρμίδη, Ειρήνη
Thesis advisor Αντωνίου, Κατερίνα
Reviewer Χαμηλός, Γεώργιος
Τσατσάνης, Χρήστος
Abstract Idiopathic pulmonary fibrosis (IPF) is the most common among the fibrosing interstitial lung diseases and is characterised by progressive deterioration of lung function and poor prognosis. The role of pulmonary macrophages in the pathogenesis of idiopathic pulmonary fibrosis remains controversial and poorly understood; although it is considered that they orchestrate the progression and maintenance of fibrosis. Impaired 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 in idiopathic pulmonary fibrosis. In this study, we used bronchoalveolar lavage (BAL), a tool for both clinical and research purposes, and a rich source of alveolar macrophages. In this study, BAL samples were examined from 52 patients with IPF and 19 healthy individuals. Measurements of mitochondria reactive oxygen species (ROS), mitochondria morphology and related gene expression were performed. Additionally, autophagy and mitophagy levels were analysed. Our results showed that mitochondria in alveolar macrophages from IPF patients have prominent morphological defects and impaired transcription. We observed a significant reduction of mitochondria homeostasis regulators PINK1, PARK2 and NRF1. Additionally, a significant increase in mitochondria ROS was associated with reduced expression of mitochondria-encoded oxidative phosphorylation (OXPHOS) genes. However, despite the increase in damaged, oxidised mitochondria, macroautophagy and mitophagy, central processes in the maintenance of healthy mitochondria levels, were not upregulated in IPF AMs. Importantly, mitochondria ROS was correlated with lung function parameters and disease severity as measured by composite physiologic index (CPI). Conclusively, our results suggest a perturbation of mitochondria homeostasis in alveolar macrophages in IPF.
Language English
Subject Mitochondria
Issue date 2019-12-11
Collection   Faculty/Department--School of Medicine--Department of Medicine--Doctoral theses
  Type of Work--Doctoral theses
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