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Effects of Chronic Kidney Disease on Oxidative Stress, Immune Deregulation, and Mitochondrial Dysfunction

Mouin Seikaly*

Airflow restriction and significant lung tissue loss are hallmarks of the progressive and incapacitating illness known as chronic obstructive pulmonary disease (COPD). Cigarette smoke has been linked to an increased oxidative burden on a variety of lung cell types, making it a major risk factor for the development of COPD. Increased reactive oxygen species (ROS) levels may have a major impact on the expression of biological molecules, the function of signalling pathways, and antioxidant defence. Large amounts of ROS are released by inflammatory cells including neutrophils and macrophages, although mitochondrial dysfunction is a key factor in ROS production because of oxidative phosphorylation. Although mitochondria are dynamic organelles, excessive oxidative stress has the ability to change their morphology, RNA content, and function. Indeed, fusion and fission, which are necessary activities to maintain a sound and functional mitochondrial network, can cause mitochondria to change their shape. These processes are regulated by the proteins mitofusin 1, mitofusin 2, and ocular atrophy 1. Smoking cigarettes can lead to mitochondrial hyperfusion, which lowers the ability of the cells to withstand stress and maintain mitochondrial quality. Additionally, decreased levels of mitophagy-related enzymes like Parkin (an ubiquitin ligase E3) and the PTEN-induced putative kinase 1 (PINK1) are frequently seen in COPD and are directly related to the disorder’s improper clearance of damaged mitochondria and subsequent cell senescence. In this review, we focus on the key mechanisms for mitochondrial quality maintenance and how oxidative stress affects them throughout the onset and progression of COPD.