Copy reference, caption or embed code

- Homocysteine and Hypertension in Diabetes: Does PPARγ Have a Regulatory Role?

Proposed mechanism of homocysteine associated hypertension in diabetes. Diabetes causes renal microvascular constriction and deposition of extracellular matrix in the glomerular basement membrane. This causes glomerulosclerosis and impaired glomerular function (GFR). Renal hypofiltration increases plasma homocysteine level, which further cause oxidative stress and amplifies glomerular injury. Increased matrix accumulation in the myocardium leads to deposition of extracellular matrix between endothelium and myocyte causing endothelium myocyte uncoupling. This causes prevention of NO to pass through the matrix barrier and impairs left ventricular diastolic dysfunction. Glomerulosclerosis and L-V diastolic dysfunction results in hypertension.
Proposed mechanism of homocysteine associated hypertension in diabetes. Diabetes causes renal microvascular constriction and deposition of extracellular matrix in the glomerular basement membrane. This causes glomerulosclerosis and impaired glomerular function (GFR). Renal hypofiltration increases plasma homocysteine level, which further cause oxidative stress and amplifies glomerular injury. Increased matrix accumulation in the myocardium leads to deposition of extracellular matrix between endothelium and myocyte causing endothelium myocyte uncoupling. This causes prevention of NO to pass through the matrix barrier and impairs left ventricular diastolic dysfunction. Glomerulosclerosis and L-V diastolic dysfunction results in hypertension.
Go to figure page
Reference
Caption
Embed code