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Profiling Ubiquitin and Ubiquitin-like Dependent Post-translational Modifications and Identification of Significant Alterations
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Ubiquitination in Scleroderma Fibrosis and Its Treatment

Ying Long1, Weilin Chen1, Qian Du1

  • 1Department of Rheumatology, Xiangya Hospital, Central South University, Changsha, China.

Frontiers in Immunology
|November 3, 2018
PubMed

Insights

This review explores ubiquitination

Area of Science:

  • Rheumatology and Immunology
  • Molecular Biology
  • Cellular Mechanisms

Background:

  • Scleroderma (systemic sclerosis, SSc) is a complex rheumatic disease characterized by organ fibrosis.
  • Transforming growth factor-β (TGF-β), WNT/β-catenin, and STAT3 pathways are implicated in SSc fibrosis.
  • Current therapies do not effectively halt or reverse SSc progression.

Purpose of the Study:

  • To review the molecular mechanisms of ubiquitination in SSc.
  • To identify potential therapeutic targets within the ubiquitination pathway for SSc treatment.

Main Methods:

  • Literature review of studies on ubiquitination in SSc.
  • Analysis of the role of ubiquitination in fibrotic processes.

Main Results:

  • Dysregulated ubiquitination is observed in fibrotic and rheumatic diseases.
  • Ubiquitination controls critical cellular functions relevant to fibrosis.
  • Few studies have investigated ubiquitination's specific role in SSc.

Conclusions:

  • Ubiquitination dysregulation is a potential contributor to SSc pathogenesis.
  • Targeting the ubiquitination pathway offers promising therapeutic avenues for SSc.
  • Further research is needed to elucidate specific mechanisms and targets.
Keywords:
SScSTAT3TGF-βWNT/β-cateninubiquitination

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