Bicknell, Katrina - University of Reading

研究领域

Coronary artery disease is the most common form of heart disease, affecting over one million people in the UK. This occurs when atherosclerotic lesions obstruct the flow of blood though the coronary vessels that supply the heart. Narrowing or blockage of these vessels leads to myocardial ischemia, which can result in angina, a heart attack (myocardial infarction), sudden cardiac death and/or heart failure. If the blood supply is not restored rapidly to the ischaemic region of the heart, myocardial infarction can result in terminal loss of cardiomyocytes, leading to permanent myocardial damage. Damaged myocardial tissue cannot be replaced, as the proliferative capacity of surviving cardiomyocytes is severely limited. Instead, within hours of the injury, cardiac remodelling is initiated and this progresses over weeks and months. Maladaptive left ventricular remodelling after myocardial infarction is a leading cause of heart failure and includes the development of cardiomyocyte hypertrophy to compensate for lost functional myocardium and replacement of the necrotic myocardial region with an inflexible scar. Thus, understanding what limits myocardial repair following injury and the development of novel therapeutic strategies to promote cardiac regeneration following myocardial infarction are of great importance. The aim of my research is to expand our understanding of the molecular mechanisms that limit cardiac repair following injury. For instance, we do not fully understand the molecular events that prevent cardiomyocyte proliferation and promote cardiac hypertrophic growth in the injured adult mammalian heart. An increased understanding of the molecular mechanisms that control cardiomyocyte growth might aid the development of therapies aimed at re-initiating myocardial cell division to repair an injured myocardium or to treat detrimental cardiac hypertrophy that can lead to heart failure.

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Swioklo, S., Watson, K. A., Williamson, E. M., Farrimond, J. A., Putnam, S. E. and Bicknell, K. A. (2015) Defining key structural determinants for the pro-osteogenic activity of flavonoids. Journal of Natural Products, 78 (11). pp. 2598-2608. ISSN 1520-6025 doi: 10.1021/acs.jnatprod.5b00075 Dannoura, A., Giraldo, A., Pereira, I., Gibbins, J., Dash, P., Bicknell, K. and Brooks, G. (2014) Ibuprofen inhibits migration and proliferation of human coronary artery smooth muscle cells by inducing a differentiated phenotype: role of peroxisome proliferator-activated receptor y. Journal of Pharmacy and Pharmacology, 66 (6). pp. 779-792. ISSN 0022-3573 doi: 10.1111/jphp.12203 Aravindan, L., Bicknell, K.A., Brooks, G., Khutoryanskiy, V.V. and Williams, A.C. (2013) A comparison of thiolated and disulfide‐crosslinked polyethylenimine for nonviral gene delivery. Macromolecular Bioscience, 13 (9). pp. 1163-1173. ISSN 1616-5187 doi: 10.1002/mabi.201300103 Moseley, F. L., Faircloth, M. E., Lockwood, W., Marber, M. S., Bicknell, K. A., Valasek, P. and Brooks, G. (2011) Limitations of the MRL mouse as a model for cardiac regeneration. Journal of Pharmacy and Pharmacology, 63 (5). pp. 648-656. ISSN 2042-7148 doi: 10.1111/j.2042-7158.2011.01261.x Aravindan, L. , Bicknell, K. A., Brooks, G., Khutoryanskiy, V. V. and Williams, A. C. (2009) Effect of acyl chain length on transfection efficiency and toxicity of polyethylenimine. International Journal of Pharmaceutics, 378 (1-2). pp. 201-210. ISSN 0378-5173 doi: 10.1016/j.ijpharm.2009.05.052 Bicknell, K. A., Harmer, S. C., Yiangson, S., Lockwood, W. and Bicknell, A. B. (2009) Lys-gamma3-MSH: a global regulator of hormone sensitive lipase activity? Molecular and Cellular Endocrinology , 300 (1-2). pp. 71-76. ISSN 0303-7207 doi: 10.1016/j.mce.2008.09.032 Coxon, C. H., Bicknell, K. A., Moseley, F. L. and Brooks, G. (2009) Over expression of Plk1 does not induce cell division in rat cardiac myocytes in vitro. PLoS ONE, 4 (8). e6752. ISSN 1932-6203 doi: 10.1371/journal.pone.0006752