Our findings suggest that variation at the angiotensin-converting enzyme gene locus is one of the factors involved in the predisposition of diabetic patients to the development of arterial disease and hypertension.
While not subject to dietary modulation, lipoprotein[a] nonetheless has provided one of the more promising leads to understanding genetic predisposition to arterial disease.
We sequenced the coding region of MS in 8 hyperhomocysteinaemic patients (4 NTD patients and 4 patients with pregnancies complicated by spiral arterial disease, SAD).
The heterozygous 20210 G/Aprothrombin genotype is associated with early venous thrombosis in inherited thrombophilias and is not increased in frequency in artery disease.
These data support the hypothesis that the prothrombin variant is a risk factor for venous thrombosis and suggest that it may also be a risk factor for arterial disease.
Although the production of MMP-1 and the proliferation of SMC are thought to play an important role in reconstruction of the intima during atherogenesis, our results suggest a possible role of IL-4 induced MMP-1 in inhibiting tissue remodeling caused by a variety of arterial disorders including atherosclerosis.
Although the production of MMP-1 and the proliferation of SMC are thought to play an important role in reconstruction of the intima during atherogenesis, our results suggest a possible role of IL-4 induced MMP-1 in inhibiting tissue remodeling caused by a variety of arterial disorders including atherosclerosis.
One hallmark of this arteriopathy due to mutations of Notch 3 gene is the presence of MRI signal abnormalities in both symptomatic and asymptomatic patients.
Recently, an autosomal dominant form of cerebral arteriopathy (CADASIL) has been described in association with a Notch3 family gene on the short arm of chromosome 19.
Another mutation, factor V Leiden, has been established as a common hereditary risk factor for venous thrombosis, but its role in arterial disease remains controversial.
And isolated reports suggest other platelet polymorphisms (GPIIb, FcgammaRIIa, P-selectin, alpha2 adrenergic receptor, transforming growth factor [TGF]beta) are risk factors for arterial disease or produce a prothrombotic phenotype.
And isolated reports suggest other platelet polymorphisms (GPIIb, FcgammaRIIa, P-selectin, alpha2 adrenergic receptor, transforming growth factor [TGF]beta) are risk factors for arterial disease or produce a prothrombotic phenotype.
C242T polymorphism was determined by restriction fragment polymorphism (RFLP) analysis in 324 patients with documented PAOD and 295 control subjects without any known arterial disease. p22 phox 242 T allele frequencies and genotype distributions were not significantly different between patients and controls; the adjusted relative risk associated with the 242 T allele was 1.14 (95% CI 0.84-1.54, P=0.39), assuming an additive effect of the T allele.
In this study, we used gene transfer of eNOS in a rabbit carotid transplant model to see whether these same effects would similarly ameliorate transplant arteriopathy.