Endoplasmic Reticulum Stress in Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a long-term and worsening lung condition that results in irreversible damage to the airways and lung tissue, causing difficulty in breathing. The development of COPD is contributed to by cellular senescence, inflammation, protease-antiprotease imbalance, epigenetic changes, oxidative stress, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, apoptosis, and cell death. Endoplasmic reticulum stress and cellular protein homeostasis are critical processes for maintaining the healthy function of cells. In response to ER stress, cells initiate a protective process called the unfolded protein response (UPR). Endoplasmic reticulum stress and UPR activation in the airways can be triggered by cigarette smoke, air pollution, bacteria, viruses, or other pathogenic microorganisms. In chronic diseases like COPD, persistent inflammation and oxidative stress can increase ER stress. This can cause continuous activation of UPR mechanisms, which can impair cell function. Chronic ER stress and insufficient protein homeostasis can lead to apoptosis and harm to lung tissue. The disruption of these vital processes, which are crucial for maintaining healthy cell functions, is a key factor in the development of chronic conditions such as COPD. Regulation of ER stress and maintaining protein balance may be a potential target for managing these diseases.