Key result
This review highlights how decreased tetrahydrobiopterin (BH4) bioavailability leads to eNOS uncoupling and endothelial dysfunction, and discusses its therapeutic potential in cardiovascular diseases.
Why the study?
Decreased BH4 bioavailability with subsequent eNOS uncoupling significantly affects the pathogenesis of endothelial dysfunction in cardiovascular disorders.
Answers are grounded in this paper and cite their sources.
Tetrahydrobiopterin (BH4) is an essential cofactor of nitric oxide synthase (NOS). In the cardiovascular system, endothelial NOS (eNOS) has a major role in maintaining vascular tone and endothelial function, as well as in mediating many other vascular protective properties. Evidence from humans and animals have demonstrated that decreased BH4 bioavailability, with subsequent uncoupling of eNOS, has significant effects on the pathogenesis of endothelial dysfunction, which is a hallmark of vascular injury in cardiovascular disorders, including hypertension, hyperlipidemia, and diabetes. In this review, we discuss the synthesis of BH4, its molecular mechanisms regulating eNOS coupling, the pathophysiologic roles of decreased BH4 bioavailability in cardiovascular diseases, and the potential therapeutic application of BH4 in clinics.
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Chen et al. (2014) conducted a review in Cardiovascular diseases (hypertension, hyperlipidemia, diabetes). Tetrahydrobiopterin (BH4) was evaluated. This review highlights how decreased tetrahydrobiopterin (BH4) bioavailability leads to eNOS uncoupling and endothelial dysfunction, and discusses its therapeutic potential in cardiovascular diseases.
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