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Regulating the regulators: transcription factors as targets for attenuating proliferative arteriopathies
1Department of Physiology, Cardiovascular Research Group, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA. mautieri@unix.temple.edu
Insights
Percutaneous transluminal coronary angioplasty (PTCA) efficacy is limited by restenosis. Targeting transcription factors offers a promising strategy to combat vascular proliferative diseases and improve long-term outcomes.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Vascular Biology
Background:
- Percutaneous transluminal coronary angioplasty (PTCA) and stenting are increasingly used for coronary artery disease.
- Vascular restenosis and allograft vasculopathy limit the long-term efficacy of these procedures.
- Current pharmacological interventions are lacking due to poor understanding of disease mechanisms.
Purpose of the Study:
- To review the cellular and molecular biology of proliferative arteriopathy.
- To summarize promising transcription factor targets for combating vascular proliferative diseases.
Main Methods:
- Literature review of cellular and molecular mechanisms in vascular proliferative diseases.
- Analysis of gene transcription and transcription factor regulation in response to vascular injury.
Main Results:
- Vascular injury induces gene transcription, driving neointimal hyperplasia and remodeling.
- Transcription factors tightly regulate this gene transcription process.
- Several transcription factors show potential as therapeutic targets.
Conclusions:
- Understanding transcription factor regulation is key to developing new treatments for vascular proliferative diseases.
- Targeting transcription factors offers a promising strategy to overcome limitations of current PTCA and stenting procedures.
Abstract:
The use of percutaneous transluminal coronary angioplasty (PTCA) and stenting to treat coronary artery disease has increased exponentially in the past decade. However, the long term efficacy of PTCA is significantly limited by the high incidence of vascular restenosis observed in as many as 30% of patients undergoing this procedure. Likewise, coronary allograft vasculopathy remains the major cause of graft failure. The lack of effective pharmacological interventions in preclinical and clinical studies is indicative of our poor understanding of the molecular mechanisms underlying vascular proliferative diseases. A wave of gene transcription is induced as part of the vascular response to injury, which initiates and maintains the progression of vascular remodeling and the neointimal hyperplasia characteristic of this disease. Because gene transcription is tightly regulated by transcription factors, they make attractive targets for combating proliferative arteriopathies. In this review, we will examine the cellular and molecular biology of proliferative arteriopathy, as well as summarize transcription factors that show promise as targets to combat vascular proliferative diseases.