COPD is a severe and debilitating lung disease that is associated with high morbidity and mortality. Currently, no curative treatments are available. In order to identify novel therapeutic targets, it is important to understand the molecular and cellular mechanisms underlying the pathogenesis of COPD. The primary focus of this seminar is to explore the metabolic alterations and cellular stress responses upon exposure to noxious particles in healthy and diseased lungs, and how these contribute to the development of COPD and its systemic manifestations. Accumulating evidence points towards a crucial role for cellular stress and alterations in the metabolic processes of structural and innate immune cells. Chronic inhalation of toxic gases and particles, including cigarette smoke, exhaust fumes, fine dust and micro- and nanoplastics induces oxidative stress and cellular damage in the lungs. In combination with genetic susceptibility and/or epigenetic modifications, this can ultimately lead to metabolic reprogramming in lung tissue as well as systemic changes with metabolic abnormalities. At cellular level, COPD lungs display mitochondrial dysfunction, DNA damage, impaired proteasomal activity and ER stress. This is associated with metabolic reprogramming, cell damage and death, and subsequent release of damage-associated molecular patterns (DAMPs), triggering immune and remodelling processes and systemic manifestations. We aim for the submission of review and research atricles that cover the latest findings in the field of metabolic alterations and cellular stress responses in COPD, including effects of cigarette smoke extract and environmental pollutants, oxidative stress responses, mitochondrial dysfunction, mitophagy, the role of novel cell death modalities such as ferroptosis, necroptosis, NETosis, DAMP release, and systemic metabolic alteration.
Date: 29 June 2022
Time: 10:00 am CEST | 4:00 am EDT | 4:00 pm CST Asia
Webinar ID: 896 1519 7776
Webinar Secretariat: cells.webinar@mdpi.com