Our objective
The end goal of our research is to develop more effective treatments for the debilitating conditions associated with vascular complications.
Our Group focuses on understanding the pathogenesis of atherosclerosis and cardiovascular disease (CVD). We use multiple models, genetic manipulation, biochemical and molecular biology tools to dissect how blood vessels become dysregulated, with particular emphasis on changes to transcriptional regulation, vascular cell adaptation and function, under normal and abnormal settings in the blood vessel wall.
Our recent work has focused on identifying protective mechanism(s) of specific genes, which have opened new opportunities for developing novel therapeutic interventions. We also ask critical questions underlying pathogenesis of obesity, diabetes and kidney disease, which are complications of CVD.
Selected publications
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.