Reprogramming the cell cycle machinery to treat cardiovascular disease

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Bicknell, K. A. orcid id iconORCID: https://orcid.org/0000-0002-5888-1424 and Brooks, G. (2008) Reprogramming the cell cycle machinery to treat cardiovascular disease. Current Opinion in Pharmacology, 8 (2). pp. 193-201. ISSN 1471-4892 doi: 10.1016/j.coph.2007.12.015

Abstract/Summary

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.

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Item Type Article
URI https://reading-clone.eprints-hosting.org/id/eprint/13787
Identification Number/DOI 10.1016/j.coph.2007.12.015
Refereed Yes
Divisions Life Sciences > School of Biological Sciences > Biomedical Sciences
Life Sciences > School of Chemistry, Food and Pharmacy > School of Pharmacy
Interdisciplinary centres and themes > Institute for Cardiovascular and Metabolic Research (ICMR)
Uncontrolled Keywords Angioplasty, Transluminal, Percutaneous Coronary/methods, Animals, Cardiovascular Diseases/*drug therapy/physiopathology, Cell Cycle/*drug effects, Coronary Artery Bypass/methods, Coronary Restenosis/prevention & control, *Drug Delivery Systems, Graft Occlusion, Vascular/prevention & control, Humans, Myocytes, Cardiac/metabolism
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