Key result
Cell cycle regulatory therapies show potential to limit post-angioplasty hyperplasia and repair post-infarction myocardium.
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In the preceding sections we have described the potential for using cell cycle regulatory molecules as targets for drug development within the cardiovascular system. Opportunities for affecting the expression and activities of selected cell cycle regulatory molecules exist in interventional cardiological procedures such as PTCA to limit specifically the intimal hyperplasia of vascular smooth muscle cells that occurs following angioplasty. In addition, the potential for targeting the cardiac myocyte cell cycle to re-initiate cell division in a controlled manner would provide a suitable approach for repairing damaged areas of myocardial tissue following an infarct. Although this approach has not been demonstrated to date in vivo, data from transgenic mouse models and in vitro studies have implicated the cell cycle as a suitable target for manipulation. The next few years will enable the feasibility of this approach to be demonstrated.
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Jian‐Mei Li (1999) conducted a review in Cardiovascular diseases (post-angioplasty intimal hyperplasia, myocardial infarction). Cell cycle regulatory molecules as therapeutic targets was evaluated. Targeting cell cycle regulatory molecules presents potential therapeutic opportunities to limit intimal hyperplasia following angioplasty and to repair damaged myocardial tissue post-infarction.
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