The Potential of Cylindromatosis (CYLD) as a Therapeutic Target in Oxidative Stress-Associated Pathologies: A Comprehensive Evaluation

Oxidative stress (OS) arises as a consequence of an imbalance between the formation of reactive oxygen species (ROS) and the capacity of antioxidant defense mechanisms to neutralize them. Excessive ROS production can lead to the damage of critical biomolecules, such as lipids, proteins, and DNA, ultimately contributing to the onset and progression of a multitude of diseases, including atherosclerosis, chronic obstructive pulmonary disease, Alzheimer's disease, and cancer. Cylindromatosis (CYLD), initially identified as a gene linked to familial cylindromatosis, has a well-established and increasingly well-characterized function in tumor inhibition and anti-inflammatory processes. Nevertheless, burgeoning evidence suggests that CYLD, as a conserved deubiquitination enzyme, also plays a pivotal role in various key signaling pathways and is implicated in the pathogenesis of numerous diseases driven by oxidative stress. In this review, we systematically examine the current research on the function and pathogenesis of CYLD in diseases instigated by oxidative stress. Therapeutic interventions targeting CYLD may hold significant promise for the treatment and management of oxidative stress-induced human diseases.

Automated summary

Oxidative stress, caused by an imbalance between reactive oxygen species (ROS) formation and antioxidant defense mechanisms, can lead to the damage of critical biomolecules and the development of various diseases. Cylindromatosis (CYLD), a gene associated with familial cylindromatosis, has a well-established role in tumor inhibition and anti-inflammatory processes. However, emerging evidence suggests that CYLD, as a deubiquitination enzyme, also plays a crucial role in key signaling pathways and is implicated in the pathogenesis of oxidative stress-driven diseases. This review systematically examines the current research on CYLD's function and pathogenesis in diseases induced by oxidative stress, and suggests that therapeutic interventions targeting CYLD may hold promise for treating such diseases.