Vol 58, No 5 (2007)
Review paper
Published online: 2007-10-16
Corticosteroids influence on angiogenesis in heart muscle
Endokrynol Pol 2007;58(5):436-439.
Abstract
The process of angiogenesis in a heart muscle is a way of providing the ischaemic myocardium with oxygen and nutritive
ingredients. This natural process called therapeutic angiogenesis has been tried in the treatment of patients with coronary
artery disease mainly. It has been seen as a chance of an effective beneficial therapy particularly in these patients for whom
pharmacological treatment is not sufficient and who are disqualified for operative methods such as the percutaneus coronary
angioplasty, or coronary bypass transplantation.
The goal of therapeutic angiogenesis is to stimulate the growth of new capillaries in a heart and, as a result, to improve the perfusion and function of a heart muscle.
The positive impact of the angiogenesis in a heart muscle is impeded in patients using corticosteroids in treatment for other illnesses. Corticosteroids inhibit the angiogenesis process on a cellular and tissue level. They decrease gene expression for VEGF, iNOS, inhibit the activity of transcriptive factors for AP-1 and NFkB. Corticosteroids cause the degradation of a pericellular matrix, inhibit the migration of macrophages and inhibit the synthesis of NO and interleukin. These activities of corticosteroids decrease the number of new vessels in a ischaemic miocardium and, consequently, worsen vascularization and progressive hypoxia.
(Pol J Endocrinol 2007; 58 (5): 436-439)
The goal of therapeutic angiogenesis is to stimulate the growth of new capillaries in a heart and, as a result, to improve the perfusion and function of a heart muscle.
The positive impact of the angiogenesis in a heart muscle is impeded in patients using corticosteroids in treatment for other illnesses. Corticosteroids inhibit the angiogenesis process on a cellular and tissue level. They decrease gene expression for VEGF, iNOS, inhibit the activity of transcriptive factors for AP-1 and NFkB. Corticosteroids cause the degradation of a pericellular matrix, inhibit the migration of macrophages and inhibit the synthesis of NO and interleukin. These activities of corticosteroids decrease the number of new vessels in a ischaemic miocardium and, consequently, worsen vascularization and progressive hypoxia.
(Pol J Endocrinol 2007; 58 (5): 436-439)
Keywords: corticosteroidsangiogenesisheart muscle