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Atherosclerosis|July 25, 1997
Stimulation of endothelial nitric oxide production by homocyst(e)ineG R Upchurch, G N Welch, A J Fabian, et al.Minerva Cardioangiologica|August 6, 2003
Organic nitrate tolerance and endothelial dysfunction: role of folate therapyJ A Leopold, J LoscalzoDrug Discovery Today. Therapeutic Strategies|November 5, 2010
Oxidative mechanisms and atherothrombotic cardiovascular diseaseJane A Leopold, Joseph LoscalzoCirculation Research|April 28, 2018
Emerging Role of Precision Medicine in Cardiovascular DiseaseJane A Leopold, Joseph LoscalzoFree Radical Biology & Medicine|September 16, 2009
Oxidative risk for atherothrombotic cardiovascular diseaseJane A Leopold, Joseph LoscalzoCurrent Atherosclerosis Reports|December 21, 2000
Oxidant stress in the vasculatureM Maytin, J Leopold, J LoscalzoVascular Medicine (London, England)|January 1, 1997
Changes in the amplitude of cyclic load biphasically modulate endothelial cell DNA synthesis and divisionG R Upchurch, J Loscalzo, A J BanesVascular Pharmacology|December 19, 2002
Vasoactive substances: nitric oxide and endothelial dysfunction in atherosclerosisGuilia Russo, Jane A Leopold, Joseph LoscalzoThe Journal of Biological Chemistry|July 4, 1997
Homocyst(e)ine decreases bioavailable nitric oxide by a mechanism involving glutathione peroxidaseG R Upchurch, G N Welch, A J Fabian, et al.Pageof 1,828