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《循环研究杂志》2005年第11期

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progesterone antagonizes the vasoprotective effect of estrogen on antioxidant enzyme expression and function
dual pathways for nuclear factor b activation by angiotensin ii in vascular smooth muscle
nadph oxidase activity and function are profoundly greater in cerebral versus systemic arteries
discrepancies between nitroglycerin and no-releasing drugs on mitochondrial oxygen consumption, vasoactivity, and the release of no
haplotype effect of the matrix metalloproteinase-1 gene on risk of myocardial infarction
embryonic even skippedecdependent muscle and heart cell fates are required for normal adult activity, heart function, and lifespan
nitric oxide regulates transforming growth factor- signaling in endothelial cells
synthetic retinoid am80 suppresses smooth muscle phenotypic modulation and in-stent neointima formation by inhibiting klf5
impaired cxcr4 signaling contributes to the reduced neovascularization capacity of endothelial progenitor cells from patients with coronary artery disease
nuclear rna foci in the heart in myotonic dystrophy
cardiac myosin-binding protein-c phosphorylation and cardiac function
activation of the endothelial store-operated isoc ca2+ channel requires interaction of protein 4.1 with trpc4
myocardin enhances smad3-mediated transforming growth factor-1 signaling in a carg box-independent manner
enhanced store overloadecinduced ca2+ release and channel sensitivity to luminal ca2+ activation are common defects of ryr2 mutations linked to ventricular tachycar..
ischemic neoangiogenesis enhanced by 2-adrenergic receptor overexpression
effects of d-4f on vasodilation and vessel wall thickness in hypercholesterolemic ldl receptorecnull and ldl receptor/apolipoprotein a-i double-knockout mice on wes..
fcriib mediates c-reactive protein inhibition of endothelial no synthase
bone morphogenetic protein signaling modulates myocardin transactivation of cardiac genes
calreticulin destabilizes glucose transporter-1 mrna in vascular endothelial and smooth muscle cells under high-glucose conditions
ca2+ influxecinduced sarcoplasmic reticulum ca2+ overload causes mitochondrial-dependent apoptosis in ventricular myocytes
intrasarcoplasmic amyloidosis impairs proteolytic function of proteasomes in cardiomyocytes by compromising substrate uptake
mobilization of bone marrowecderived cells enhances the angiogenic response to hypoxia without transdifferentiation into endothelial cells
platelet-derived growth factor d induces cardiac fibrosis and proliferation of vascular smooth muscle cells in heart-specific transgenic mice
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