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Updated: Apr 3, 2026

Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease
Published on: June 16, 2020
Systemic sclerosis-associated fibrosis: an accelerated aging phenotype?
Tracy R Luckhardt1, Victor J Thannickal
1aDivision of Pulmonary, Allergy and Critical Care Medicine bDepartment of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Aging processes, including cellular senescence and immune dysregulation, may contribute to systemic sclerosis (SSc) fibrosis. Understanding these age-related cellular changes is crucial for SSc research.
Area of Science:
- Immunology
- Geroscience
- Rheumatology
Background:
- Systemic sclerosis (SSc) is an autoimmune disease characterized by multi-organ fibrosis.
- SSc-associated fibrosis exhibits similarities to age-related fibrotic disorders.
- The role of aging in SSc development is increasingly recognized.
Purpose of the Study:
- To review the current literature on the potential role of aging and age-related cellular processes in SSc.
- To explore the connection between aging mechanisms and fibrosis in systemic sclerosis.
Main Methods:
- Literature review of current research on aging and SSc.
- Analysis of cellular processes implicated in both aging and SSc fibrosis.
Main Results:
- Evidence suggests immune dysregulation, epigenetic modifications, cellular senescence, mitochondrial dysfunction, and impaired autophagy contribute to fibrosis in aging and SSc.
- These age-related cellular alterations are implicated in the development and progression of SSc-associated fibrosis.
Conclusions:
- Cellular alterations associated with aging may play a significant role in the pathogenesis and advancement of SSc-associated fibrosis.
- Further research into these age-related mechanisms could offer new therapeutic targets for SSc.
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