Reprogramming the cell cycle machinery to treat cardiovascular disease.
Coronary artery disease is one of the most common heart pathologies. Restriction of blood flow to the heart by atherosclerotic lesions, leading to angina pectoris and myocardial infarction, damages the heart, resulting in impaired cardiac function. Damaged myocardium is replaced by scar tissue since surviving cardiomyocytes are unable to proliferate to replace lost heart tissue. Although narrowing of the coronary arteries can be treated successfully using coronary revascularisation procedures, re-occlusion of the treated vessels remains a significant clinical problem. Cell cycle control mechanisms are key in both the impaired cardiac repair by surviving cardiomyocytes and re-narrowing of treated vessels by maladaptive proliferation of vascular smooth muscle cells. Strategies targeting the cell cycle machinery in the heart and vasculature offer promise both for the improvement of cardiac repair following MI and the prevention of restenosis and bypass graft failure following revascularisation procedures.
Bicknell
Katrina A
KA
Cardiovascular Research Group, Reading School of Pharmacy, University of Reading, PO Box 226, Whiteknights, Reading, Berkshire RG6 6AP, UK.
Brooks
Gavin
G
D015906:Angioplasty, Balloon, Coronary / Q000379:methods; D000818:Animals; D002318:Cardiovascular Diseases / Q000188:drug therapy* / Q000503:physiopathology; D002453:Cell Cycle / Q000187:drug effects*; D001026:Coronary Artery Bypass / Q000379:methods; D023903:Coronary Restenosis / Q000517:prevention & control; D016503:Drug Delivery Systems; D006083:Graft Occlusion, Vascular / Q000517:prevention & control; D006801:Humans; D032383:Myocytes, Cardiac / Q000378:metabolism