David A. Ford, Ph.D.
Biochemical mechanisms responsible for the pathophysiological sequelae of cardiovascular diseases, including ischemic heart disease and atherosclerosis.
Office: DRC, Room 325
Phone: (314) 977-9264
Ph.D., 1985, University of Missouri-Columbia
We are interested in biochemical mechanisms responsible for the pathophysiological sequelae of cardiovascular diseases including ischemic heart disease and atherosclerosis. Areas of research focus on enzymic and free radical targeting of membrane phospholipids, alterations in lipid metabolism, and alterations in signaling pathways as mechanisms involved in cardiovascular diseases. We combine our expertise using physiological models of disease coupled with expertise in mass spectrometry and bioorganic techniques to reveal new mechanistic insights into cardiovascular disease.
- Akt-mediated FoxO1 inhibition is required for liver regeneration.
Pauta M, Rotllan N, et al. Hepatology. (2015) [Epub ahead of print].
- Identification of glutathione adducts of alpha-chlorofatty aldehydes produced in activated neutrophils.
Duerr MA, Aurora R, Ford DA. J Lipid Res. (2015) 56(5):1014-1024.
- Lpcat3-dependent production of arachidonoly phospholipids is a key determinant of triglyceride secretion.
Rong X, Wang B, et al. Elife. (2015) 4:e06557.
- Dipeptidyl peptidase-4 inhibition ameliorates western diet-induced hepatic steatosis and insulin resistance through hepatic lipid remodeling and modulation of hepatic mitochondrial function.
Aroor AR, Habibi J, et al. Diabetes. (2015) 64(6):1988-2001.
- PON3 knockout mice are susceptible to obesity, gallstone formation, and atherosclerosis.
Shih DM, Yu JM, et al. FASEB J. (2015) 29(4):1185-1197.
- ABCG1 is required for pulmonary B-1 B cell and natural antibody homeostasis.
Baldan A, Gonen A, et al. J Immunol. (2014) 193(11):5637-5648.
- Inhibiting monoacylglycerol acyltransferase 1 ameliorates hepatic metabolic abnormalities, but not inflammation and injury in mice.
Soufi N, Hall AM, et al. J Biol Chem. (2014) 289(43):1834-1842.
- Alpha-chlorofatty acid and coronary artery or aorta calcium scores in women with systemic lupus erythematosus. A pilot study.
Mahieu MA, Guild CP, et al. J Rheumatol. (2014) 41(9):1834-1842.
- Lipidomic analyses of female mice lacking hepatic lipase and endothelial lipase indicate selective modulation of plasma lipid species.
Yang Y, Kuwano T, et al. Lipids. (2014) 49(6):505-515.
- Elaidic acid increases hepatic lipogenesis by mediating sterol regulatory element binding protein-1c activity in HuH-7 cells.
Shao F, Ford DA. Lipids. (2014) 49(5):403-413.
- Oxidation of plasmalogen, low-density lipoprotein and RAW 264.7 cells by photoactivatable atomic oxygen precursors.
Bourdillon MT, Ford BA, et al. Photochem Photobiol. (2014) 90(2):386-393.
- Alpha-chlorofatty acid accumulates in activated monocytes and causes apoptosis through reactive oxygen species production and endoplasmic reticulum stress.
Wang WY, Albert CJ, et al. Arterioscler Thromb Vasc Biol (2014) 34(3):526-532.