| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10953791 | Journal of Molecular and Cellular Cardiology | 2012 | 8 Pages |
Abstract
⺠Effects of hyperhomocysteinemia on myocardium are not well understood. ⺠Ischemia-reperfusion caused worse injury in hyperhomocysteinemic mice. ⺠Homocysteine impaired contractility and promoted apoptosis in cardiomyocytes. ⺠Mechanism is via activation of p38MAPK and increase in oxidant stress. ⺠Overexpression of thioredoxin decreased oxidant stress and rescued cardiomyocytes.
Keywords
CBSTerminal dUTP nick-end labelingHHcyTTETrxEDPHcyESPI/RROS[Ca2 +]iIschemia reperfusion injuryAntioxidantContractilityTrans-thoracic echocardiographyIschemia reperfusioncardiovascular diseaseOxidative stressTUNELthioredoxintHcyApoptosisCVDcystathionine β-synthaseCardiomyocyteswild typeNitric oxidetotal homocysteinehomocysteineHyperhomocysteinemiaEnd diastolic pressureIntracellular calciumReactive oxygen species
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Authors
Xu Wang, Lei Cui, Jacob Joseph, Bingbing Jiang, David Pimental, Diane E. Handy, Ronglih Liao, Joseph Loscalzo,