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Fibroblast and endothelial apoptosis in systemic sclerosis
Jae-Bum Jun1, Melanie Kuechle, John M Harlan
1Division of Rheumatology, Hospital for Rheumatic Diseases, Hanyang University School of Medicine, Seoul, Republic of Korea.
Current Opinion in Rheumatology
|October 22, 2003
Summary
Systemic sclerosis involves vascular and skin changes. Fibroblast resistance to apoptosis and vascular endothelial cell injury may drive disease progression, offering new therapeutic targets.
Area of Science:
- Pathophysiology of Systemic Sclerosis
- Cell Biology
- Fibrosis Research
Background:
- Systemic sclerosis is characterized by vascular and skin abnormalities, fibroblast activation, and excessive matrix synthesis.
- These lead to fibrosis and organ dysfunction (lung, kidney, GI tract).
- Emerging evidence points to vascular endothelium injury and defective fibroblast apoptosis in disease development.
Purpose of the Study:
- To review recent findings on apoptosis in vascular endothelium and skin fibroblasts in systemic sclerosis.
- To discuss the role of cell death and survival mechanisms in the disease context.
Main Methods:
- Literature review of recent studies on apoptosis in systemic sclerosis.
- Discussion of cell death paradigms in wound healing and keloid formation.
- Analysis of findings on fibroblast resistance to Fas-mediated apoptosis and Akt activation.
Main Results:
- Systemic sclerosis fibroblasts exhibit resistance to Fas-mediated apoptosis.
- Activation of the antiapoptotic protein kinase Akt may contribute to fibroblast selection in this disease.
- Defective apoptosis in vascular endothelium and fibroblasts are key areas of investigation.
Conclusions:
- Understanding death and survival signals in endothelial cells and fibroblasts is crucial.
- This knowledge is expected to pave the way for novel therapeutic strategies for systemic sclerosis.