期刊
ANTIOXIDANTS & REDOX SIGNALING
卷 9, 期 11, 页码 1911-1921出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2007.1795
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资金
- NHLBI NIH HHS [R01 HL058955] Funding Source: Medline
- NIGMS NIH HHS [R01 GM024908, R01 GM024908-27, R37 GM024908] Funding Source: Medline
Mouse models that perturb homocysteine metabolism, including genetic mouse models that result in deficiencies of methylenetetrahydrofolate reductase, methionine synthase, methionine synthase reductase, and cystathionine ss-synthase, and a pharmaceutically induced mouse model with a transient deficiency in betainehomocysteine methyl transferase, have now been characterized and can be compared. Although each of these enzyme deficiencies is associated with moderate to severe hyperhomocyst(e)inemia, the broader metabolic profiles are profoundly different. In particular, the various models differ in the degree to which tissue ratios of S-adenosylmethionine to S-adenosylhomocysteine are reduced in the face of elevated plasma homocyst(e)ine, and in the distribution of the tissue folate pools. These different metabolic profiles illustrate the potential complexities of hyperhomocyst(e)inemia in humans and suggest that comparison of the disease phenotypes of the various mouse models may be extremely useful in dissecting the underlying risk factors associated with human hyperhomocyst(e)inemia.
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