scholarly journals The emerging role of asymmetric dimethylarginine as a novel cardiovascular risk factor

2003 ◽  
Vol 59 (4) ◽  
pp. 824-833 ◽  
Author(s):  
R BOGER
Keyword(s):  
Risk Factor ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factor ◽  
Asymmetric Dimethylarginine

The role of glucose as an independent cardiovascular risk factor

2007 ◽  
Vol 7 (1) ◽  
pp. 43-49 ◽  
Author(s):  
R. Jan-Willem Middelbeek ◽  
Edward S. Horton
Keyword(s):  
Risk Factor ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factor

scholarly journals Multiple roles of haem in cystathionine b-synthase activity: implications for hemin and other therapies of acute hepatic porphyria

2021 ◽  
Author(s):  
Abdulla A-B Badawy
Keyword(s):  
Enzyme Activity ◽  
Risk Factor ◽  
Cardiovascular Risk ◽  
Cardiovascular Risk Factor ◽  
Vitamin B6 ◽  
Kynurenine Pathway ◽  
Multiple Roles ◽  
Vitamin B6 Deficiency ◽  
Haem Oxygenase

The role of haem in the activity of cystathionine b-synthase (CBS) is reviewed and a hypothesis postulating multiple effects of haem on enzyme activity under conditions of haem excess or deficiency is proposed, with implications for some therapies of acute hepatic porphyrias. CBS utilises both haem and pyridoxal 5¢-phosphate (PLP) as cofactors.  Although haem does not participate directly in the catalytic process, it is vital for PLP binding to the enzyme and potentially also for CBS stability.  Haem deficiency can therefore undermine CBS activity by impairing PLP binding and facilitating CBS degradation.  Excess haem can also impair CBS activity by inhibiting it via CO resulting from haem induction of haem oxygenase, and by induction of a functional vitamin B6 deficiency following activation of hepatic tryptophan 2,3-dioxygenase and subsequent utilisation of PLP by enhanced kynurenine aminotransferase and kynureninase activities.  CBS inhibition results in accumulation of the cardiovascular risk factor homocysteine (Hcy) and evidence is emerging for plasma Hcy elevation in patients with acute hepatic porphyrias.  Decreased CBS activity may also induce a proinflammatory state, inhibit expression of haem oxygenase and activate the extrahepatic kynurenine pathway thereby further contributing to the Hcy elevation. The hypothesis predicts likely changes in CBS activity and plasma Hcy levels in untreated hepatic porphyria patients and in those receiving hemin or certain gene-based therapies. In the present review, these aspects are discussed, means of testing the hypothesis in preclinical experimental settings and porphyric patients are suggested and potential nutritional and other therapies are proposed.

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