Ubiquitination in Scleroderma Fibrosis and Its Treatment.
Scleroderma (systemic sclerosis, SSc) is a highly heterogeneous rheumatic disease, and uncontrolled fibrosis in visceral organs is the major cause of death in patients. The transforming growth factor-β (TGF-β) and WNT/β-catenin signaling pathways, along with signal transducer and activator of transcription 3 (STAT3), play crucial roles in this fibrotic process. Currently, no therapy is available that effectively arrests or reverses the progression of fibrosis in patients with SSc. Ubiquitination is an important post-translational modification that controls many critical cellular functions. Dysregulated ubiquitination events have been observed in patients with systemic lupus erythematosus, rheumatoid arthritis and fibrotic diseases. Inhibitors targeting the ubiquitination pathway have considerable potential for the treatment of rheumatic diseases. However, very few studies have examined the role and mechanism of ubiquitination in patients with SSc. In this review, we will summarize the molecular mechanisms of ubiquitination in patients with SSc and explore the potential targets for treatment.
['Long|Ying|Y|', 'Chen|Weilin|W|', 'Du|Qian|Q|', 'Zuo|Xiaoxia|X|', 'Zhu|Honglin|H|']
D000818:Animals D015415:Biomarkers D019468:Disease Management D005355:Fibrosis D005786:Gene Expression Regulation D006801:Humans D009154:Mutation D012595:Scleroderma, Systemic D015398:Signal Transduction D054875:Ubiquitination D014452:Ubiquitins
ubiquitination SSc TGF-β WNT/β-catenin STAT3