CCN1: a SASPy protein that plays multifaceted roles in fibrogenesis
1College of Dentistry, University of Saskatchewan, Saskatoon SK S7N 5E4, Canada.
Matrix Biology : Journal of the International Society for Matrix Biology
|November 28, 2025
Summary
The matricellular protein CCN1 can induce cell death and the senescence-associated secretory phenotype (SASP). Its dual role in fibrosis, promoting or inhibiting it based on context, is crucial for developing anti-fibrotic therapies.
Area of Science:
- Cell biology
- Tissue repair
- Fibrosis research
Background:
- Matricellular protein CCN1 is implicated in cellular processes like apoptosis and senescence.
- The senescence-associated secretory phenotype (SASP) contributes to tissue repair but can cause pathological fibrosis if clearance is impaired.
- CCN1 exhibits context-dependent roles in fibrosis, acting both anti-fibrotically and pro-fibrotically.
Purpose of the Study:
- To explore the multifaceted roles of CCN1 in cellular processes.
- To investigate the context-dependent functions of CCN1 in various fibrotic conditions.
- To inform the development of targeted anti-fibrotic drugs.
Main Methods:
- Review of recent scientific literature on CCN1 and fibrosis.
- Analysis of CCN1's pro-apoptotic and SASP-inducing capabilities.
- Examination of CCN1's role in different fibrotic models (liver, lung, kidney, cardiac, skin).
Main Results:
- CCN1 is a potential inducer of apoptosis and SASP.
- CCN1 demonstrates anti-fibrotic activity in normal tissue repair and liver contexts.
- CCN1 exhibits pro-fibrotic activity in lung, kidney, cardiac, and skin fibrosis, and also in liver scarring.
Conclusions:
- CCN1's dual role in fibrosis necessitates careful consideration in therapeutic strategies.
- Understanding the context-specific functions of CCN1 is vital for effective anti-fibrotic drug development.
- Further research into CCN1's mechanisms in different fibrotic diseases is warranted.
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