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

• Published in: International journal of molecular sciences 2023-05, Vol.24 (9), p.8368
• Main Authors: Huang, Zhenzhou, Tan, Yanjie
• Format: Article
• Language: English
• Subjects: Alzheimer's disease; Amino acids; Apoptosis; Arteriosclerosis; Atherosclerosis; Biomolecules; Cancer; Cardiovascular disease; Cell cycle; Cell growth; Chronic obstructive pulmonary disease; CYLD; Deubiquitinating Enzyme CYLD - genetics; Deubiquitinating Enzyme CYLD - metabolism; deubiquitination; Development and progression; disease; DNA damage; Gene expression; Genetic aspects; Health aspects; Humans; Inflammation; Kidney diseases; Kinases; Lipids; Localization; Lung diseases; Lung diseases, Obstructive; Obesity; Obstructive lung disease; Oxidation; Oxidation-Reduction; Oxidative Stress; Pathogenesis; Phosphorylation; Proteins; Reactive oxygen species; Reactive Oxygen Species - metabolism; Review; Signal Transduction; Therapeutic applications; Therapeutic targets; Traumatic brain injury; Tumorigenesis; Tumors
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms24098368

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.