Matches in SemOpenAlex for { <https://semopenalex.org/work/W2159922182> ?p ?o ?g. }
- W2159922182 endingPage "672" @default.
- W2159922182 startingPage "645" @default.
- W2159922182 abstract "Based on recent retrospective, prospective, and experimental studies, mild to moderate elevation of fasting or postmethionine-load plasma homocysteine is accepted as an independent risk factor for cardiovascular disease and thrombosis in both men and women. Hyperhomocysteinemia results from an inhibition of the remethylation pathway or from an inhibition or a saturation of the transsulfuration pathway of homocysteine metabolism. The involvement of a high dietary intake of methionine-rich animal proteins has not yet been investigated and cannot be ruled out. However, folate deficiency, either associated or not associated with the thermolabile mutation of the N(5,10)-methylenetetrahydrofolate reductase, and vitamin B(6) deficiency, perhaps associated with cystathionine beta-synthase defects or with methionine excess, are believed to be major determinants of the increased risk of cardiovascular disease related to hyperhomocysteinemia. Recent experimental studies have suggested that moderately elevated homocysteine levels are a causal risk factor for atherothrombotic disease because they affect both the vascular wall structure and the blood coagulation system. The oxidant stress that results from impaired homocysteine metabolism, which modifies the intracellular redox status, might play a central role in the molecular mechanisms underlying moderate hyperhomocysteinemia-mediated vascular disorders. Because folate supplementation can efficiently reduce plasma homocysteine levels, both in the fasting state and after methionine loading, results from further prospective cohort studies and from on-going interventional trials will determine whether homocysteine-lowering therapies can contribute to the prevention and reduction of cardiovascular risk. Additionally, these studies will provide unequivocal arguments for the independent and causal relationship between hyperhomocysteinemia and atherothrombotic disease." @default.
- W2159922182 created "2016-06-24" @default.
- W2159922182 creator A5024777189 @default.
- W2159922182 creator A5037595813 @default.
- W2159922182 creator A5067980467 @default.
- W2159922182 creator A5080864887 @default.
- W2159922182 creator A5086777435 @default.
- W2159922182 date "2001-05-01" @default.
- W2159922182 modified "2023-10-16" @default.
- W2159922182 title "Impaired Homocysteine Metabolism and Atherothrombotic Disease" @default.
- W2159922182 cites W112879263 @default.
- W2159922182 cites W1496335343 @default.
- W2159922182 cites W1513020808 @default.
- W2159922182 cites W1525040400 @default.
- W2159922182 cites W1550178542 @default.
- W2159922182 cites W1553491209 @default.
- W2159922182 cites W1557771952 @default.
- W2159922182 cites W1562522900 @default.
- W2159922182 cites W1611625030 @default.
- W2159922182 cites W1664335312 @default.
- W2159922182 cites W1786911182 @default.
- W2159922182 cites W1791153000 @default.
- W2159922182 cites W1793327536 @default.
- W2159922182 cites W1824744945 @default.
- W2159922182 cites W1830747593 @default.
- W2159922182 cites W1842723757 @default.
- W2159922182 cites W1860367105 @default.
- W2159922182 cites W186105450 @default.
- W2159922182 cites W1874911532 @default.
- W2159922182 cites W1890248538 @default.
- W2159922182 cites W1920696740 @default.
- W2159922182 cites W1928338006 @default.
- W2159922182 cites W1937693126 @default.
- W2159922182 cites W1940017769 @default.
- W2159922182 cites W1946849146 @default.
- W2159922182 cites W1948500600 @default.
- W2159922182 cites W1949043027 @default.
- W2159922182 cites W1963480212 @default.
- W2159922182 cites W1964761495 @default.
- W2159922182 cites W1965029028 @default.
- W2159922182 cites W1965785232 @default.
- W2159922182 cites W1966292733 @default.
- W2159922182 cites W1967900055 @default.
- W2159922182 cites W1968688007 @default.
- W2159922182 cites W1971277158 @default.
- W2159922182 cites W1974386893 @default.
- W2159922182 cites W1974871007 @default.
- W2159922182 cites W1975357252 @default.
- W2159922182 cites W1976692919 @default.
- W2159922182 cites W1977357923 @default.
- W2159922182 cites W1978796955 @default.
- W2159922182 cites W1980588491 @default.
- W2159922182 cites W1981201921 @default.
- W2159922182 cites W1981731904 @default.
- W2159922182 cites W1982341626 @default.
- W2159922182 cites W1982868620 @default.
- W2159922182 cites W1982894405 @default.
- W2159922182 cites W1983823485 @default.
- W2159922182 cites W1985252254 @default.
- W2159922182 cites W1985846516 @default.
- W2159922182 cites W1985987751 @default.
- W2159922182 cites W1986519649 @default.
- W2159922182 cites W1988922797 @default.
- W2159922182 cites W1989929999 @default.
- W2159922182 cites W1989964772 @default.
- W2159922182 cites W1990926399 @default.
- W2159922182 cites W1991988518 @default.
- W2159922182 cites W1993145269 @default.
- W2159922182 cites W1994044028 @default.
- W2159922182 cites W1994512857 @default.
- W2159922182 cites W1994591574 @default.
- W2159922182 cites W1995630164 @default.
- W2159922182 cites W1995781460 @default.
- W2159922182 cites W1997596609 @default.
- W2159922182 cites W1998807979 @default.
- W2159922182 cites W2001163783 @default.
- W2159922182 cites W2002660287 @default.
- W2159922182 cites W2004520880 @default.
- W2159922182 cites W2006845245 @default.
- W2159922182 cites W2007242048 @default.
- W2159922182 cites W2007371357 @default.
- W2159922182 cites W2010202776 @default.
- W2159922182 cites W2010761547 @default.
- W2159922182 cites W2011477467 @default.
- W2159922182 cites W2011536055 @default.
- W2159922182 cites W2019468493 @default.
- W2159922182 cites W2020649932 @default.
- W2159922182 cites W2020802956 @default.
- W2159922182 cites W2020902432 @default.
- W2159922182 cites W2021395497 @default.
- W2159922182 cites W2021905990 @default.
- W2159922182 cites W2022553195 @default.
- W2159922182 cites W2022938812 @default.
- W2159922182 cites W2023495150 @default.
- W2159922182 cites W2023719852 @default.
- W2159922182 cites W2026483758 @default.
- W2159922182 cites W2026967560 @default.
- W2159922182 cites W2027607346 @default.