Our mission is to understand the pathogenesis of blood vessel disease and its complications, and using this knowledge, identify new strategies to improve the burden of cardiovascular disease (CVD) in people.
Our research uses various models, genetic manipulation, and biochemical and molecular biology tools to dissect how blood vessels become dysregulated, with an emphasis on changes to gene expression, vascular cell adaptation and function in both normal and abnormal settings in the blood vessel wall.
Our research aims to understand the molecular, biochemical and cellular mechanisms underlying blood vessel diseases, focusing on atherosclerosis and its complications, including peripheral vascular disease and diabetes. By providing new knowledge as to how blood vessels become dysregulated in CVD and related pathologies, our work will help uncover new strategies and therapeutics to combat disease, ultimately improving quality of life and life expectancy.
Ravindran D, et al. Broad-spectrum Chemokine Inhibition Blocks Inflammation-Induced Angiogenesis, but Preserves Ischemia-Driven Angiogenesis. FASEB J. 2019 Dec. 33 (12), 13423-13434. DOI: 10.1096/fj.201900232RR
Nash M, et al. TNF superfamily members in ischaemic vascular diseases. Cardiovasc Res. 2019 Feb 28. pii: cvz042. doi: 10.1093/cvr/cvz042.
Cartland SP, et al. TRAIL-expressing monocyte/macrophages are critical for reducing inflammation and atherosclerosis. iScience, 2019 Feb 22;12:41-52. doi: 10.1016/j.isci.2018.12.037. Epub 2019 Jan 4.
Cholan P, et al. TRAIL protects against endothelial dysfunction in vivo and inhibits angiotensin-II induced oxidative stress in vascular endothelial cells in vitro. Free Rad Biol Med; accepted August 27, 2018.
Cholan P, et al. NADPH Oxidases, angiogenesis and peripheral artery disease. Antioxidants (2017).;6(3). pii: E56. doi: 10.3390/antiox6030056.
Cartland SP, et al. Non-alcoholic fatty liver disease is exacerbated with TRAIL deletion in mice, associating with vascular inflammation and insulin resistance. Sci Reports (2017):7(1):1898.