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Growth factors and endothelial dysfunction
1Cardiology B Department and Pharmacology Laboratory, Lille University Hospital, France.
Insights
Endothelial dysfunction contributes to cardiovascular diseases. Growth factors like basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) improve endothelial function and vessel repair, offering a potential therapeutic strategy.
Area of Science:
- Cardiovascular Research
- Vascular Biology
- Regenerative Medicine
Background:
- Endothelial dysfunction is central to cardiovascular diseases, affecting arterial vasomotion, thrombosis, and neointimal proliferation.
- It is a hallmark of atherosclerosis, mechanically injured arteries, and collateral vessels in ischemia.
- Endothelial cells rely on growth factors like fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF) for in vitro growth.
Purpose of the Study:
- To investigate the therapeutic potential of endothelial cell growth factors in vivo.
- To explore the role of FGF and VEGF in improving endothelial dysfunction.
- To assess the impact of these factors on vascular repair and function.
Main Methods:
- Administration of basic FGF (bFGF) and VEGF in animal models of endothelial dysfunction.
- Evaluation of collateral vessel development in ischemic models.
- Assessment of endothelial regrowth after arterial injury.
- Analysis of endothelium-dependent responses in various disease models.
Main Results:
- In vivo administration of bFGF and VEGF enhanced collateral vessel formation in ischemic conditions.
- These growth factors promoted endothelial regrowth following arterial injury.
- Significant improvements in endothelium-dependent responses were observed in animal models of endothelial dysfunction.
- Beneficial effects were noted in models of collateral circulation, arterial injury, and atherosclerosis.
Conclusions:
- Endothelial cell growth factors, including bFGF and VEGF, demonstrate significant therapeutic potential.
- These factors improve vascular function and repair mechanisms in various models of endothelial dysfunction.
- Further research into the precise mechanisms is warranted, but these findings support their use in treating vascular diseases.
Abstract:
Endothelial dysfunction has been implicated in the pathogenesis of many cardiovascular diseases; experimental and clinical studies have shown that endothelial dysfunction may be a key factor in various processes, including abnormal arterial vasomotion, thrombosis or neointimal proliferation. Endothelial dysfunction has been shown to be a characteristic feature of atherosclerotic vessels, sites subject to mechanical injury or collateral vessels that develop in response to severe ischaemia. Fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF) are important growth factors for endothelial cells in vitro. While VEGF is specific for endothelial cells, FGFs are also potent growth factors for other cell types such as smooth muscle cells. Recent studies have demonstrated the feasibility of using endothelial cell growth factors in vivo. Basic FGF (bFGF) and VEGF have been shown to increase the development of collateral vessels in ischaemic models and to enhance the extent of endothelial regrowth following arterial injury. The marked anatomical improvement associated with the administration of endothelial cell growth factors has promoted questions concerning a possible role for these factors in endothelial dysfunction. In vivo administration of endothelial cell growth factors is associated with significant improvement in endothelium-dependent responses. This effect is observed with bFGF and VEGF in various animal models of endothelial dysfunction such as the collateral circulation, the regenerated endothelium following arterial injury and experimental atherosclerosis. While the precise mechanisms underlying this ubiquitous beneficial effect of endothelial cell growth factors are still to be determined, these results do support the concept of using such factors as a new therapeutic strategy in patients with vascular diseases.