Nitrative inactivation of thioredoxin-1 increases vulnerability of diabetic hearts to ischemia/reperfusion injury.
about
Interplay of oxidative, nitrosative/nitrative stress, inflammation, cell death and autophagy in diabetic cardiomyopathyThioredoxins, glutaredoxins, and peroxiredoxins--molecular mechanisms and health significance: from cofactors to antioxidants to redox signalingBioinformatics analysis reveals biophysical and evolutionary insights into the 3-nitrotyrosine post-translational modification in the human proteomeHydrogen sulfide preconditions the db/db diabetic mouse heart against ischemia-reperfusion injury by activating Nrf2 signaling in an Erk-dependent mannerIntralipid, a clinically safe compound, protects the heart against ischemia-reperfusion injury more efficiently than cyclosporine-A.Inhibition of ALDH2 by O-GlcNAcylation contributes to the hyperglycemic exacerbation of myocardial ischemia/reperfusion injury.Interacting with thioredoxin-1--disease or no disease?Oxidative stress and myocardial injury in the diabetic heartTyrosine nitration as mediator of cell death.Thioredoxin superfamily and its effects on cardiac physiology and pathology.Nitrosative Stress, Hypernitrosylation, and Autoimmune Responses to Nitrosylated Proteins: New Pathways in Neuroprogressive Disorders Including Depression and Chronic Fatigue Syndrome.The Impact of Environmental Factors in Influencing Epigenetics Related to Oxidative States in the Cardiovascular System.The expanding world of post-translational modifications.Cardiac-derived adiponectin induced by long-term insulin treatment ameliorates myocardial ischemia/reperfusion injury in type 1 diabetic mice via AMPK signaling.Notch1 cardioprotection in myocardial ischemia/reperfusion involves reduction of oxidative/nitrative stress.A soluble receptor for advanced glycation end-products inhibits myocardial apoptosis induced by ischemia/reperfusion via the JAK2/STAT3 pathway.Reduction in IL-33 expression exaggerates ischaemia/reperfusion-induced myocardial injury in mice with diabetes mellitus.Tongxinluo attenuates reperfusion injury in diabetic hearts by angiopoietin-like 4-mediated protection of endothelial barrier integrity via PPAR-α pathway.
P2860
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P2860
Nitrative inactivation of thioredoxin-1 increases vulnerability of diabetic hearts to ischemia/reperfusion injury.
description
2010 nî lūn-bûn
@nan
2010年の論文
@ja
2010年学术文章
@wuu
2010年学术文章
@zh
2010年学术文章
@zh-cn
2010年学术文章
@zh-hans
2010年学术文章
@zh-my
2010年学术文章
@zh-sg
2010年學術文章
@yue
2010年學術文章
@zh-hant
name
Nitrative inactivation of thio ...... o ischemia/reperfusion injury.
@en
Nitrative inactivation of thio ...... o ischemia/reperfusion injury.
@nl
type
label
Nitrative inactivation of thio ...... o ischemia/reperfusion injury.
@en
Nitrative inactivation of thio ...... o ischemia/reperfusion injury.
@nl
prefLabel
Nitrative inactivation of thio ...... o ischemia/reperfusion injury.
@en
Nitrative inactivation of thio ...... o ischemia/reperfusion injury.
@nl
P2093
P1476
Nitrative inactivation of thio ...... to ischemia/reperfusion injury
@en
P2093
Haichang Wang
Shaowei Liu
P304
P356
10.1016/J.YJMCC.2010.05.002
P577
2010-05-16T00:00:00Z