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cystathionine/hypoxia

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Hypoxia-inducible factors regulate human and rat cystathionine β-synthase gene expression.

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Increased catalytic activity of CBS (cystathionine β-synthase) was recently shown to mediate vasodilation of the cerebral microcirculation, which is initiated within minutes of the onset of acute hypoxia. To test whether chronic hypoxia was a stimulus for increased CBS expression, U87-MG human

The cystathionine γ-lyase/hydrogen sulfide pathway mediates the trimetazidine-induced protection of H9c2 cells against hypoxia/reoxygenation-induced apoptosis and oxidative stress.

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Trimetazidine is a piperazine-derived metabolic agent. It exerts cardioprotective effects against myocardial ischemia/reperfusion (I/R) injury. In addition, studies confirm that the cystathionine γ-lyase (CSE)/hydrogen sulfide (H2S) pathway serves a beneficent role in attenuating

Regulation of cystathionine γ-lyase in mammalian cells by hypoxia.

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Hydrogen sulfide (H2S), an endogenous signaling molecule in mammalian cells, shows a variety of biological effects. Cystathionine γ-lyase (CSE) is a key enzyme in the trans-sulfuration pathway responsible for the production of endogenous H2S. Whether CSE expression is regulated by hypoxia in

3-Mercaptopyruvate Sulfurtransferase, Not Cystathionine β-Synthase Nor Cystathionine γ-Lyase, Mediates Hypoxia-Induced Migration of Vascular Endothelial Cells.

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Hypoxia-induced angiogenesis is a common phenomenon in many physiological and patho-physiological processes. However, the potential differential roles of three hydrogen sulfide producing systems cystathionine γ-lyase (CSE)/H2S, cystathionine β-synthase (CBS)/H2S, and 3-mercaptopyruvate

NFAT regulation of cystathionine γ-lyase expression in endothelial cells is impaired in rats exposed to intermittent hypoxia.

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Sleep apnea is a risk factor for cardiovascular disease, and intermittent hypoxia (IH, 20 episodes/h of 5% O2-5% CO2 for 7 h/day) to mimic sleep apnea increases blood pressure and impairs hydrogen sulfide (H2S)-induced vasodilation in rats. The enzyme that produces H2S, cystathionine γ-lyase (CSE),

Role of cystathionine-γ-lyase in hypoxia-induced changes in TASK activity, intracellular [Ca2+] and ventilation in mice.

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Cystathionine-γ-lyase (CSE) is a multifunctional enzyme, and hydrogen sulfide (H2S) is one of its products. CSE and H2S have recently been proposed to be critical signaling molecules in hypoxia-induced excitation of carotid body (CB) glomus cells and the chemosensory response. Because the role of

Protective action of endogenously generated H₂S on hypoxia-induced respiratory suppression and its relation to antioxidation and down-regulation of c-fos mRNA in medullary slices of neonatal rats.

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We previously reported that exogenous H(2)S played roles in protection of respiratory centers against hypoxic injury in medullary slices of neonatal rats. The protective action of endogenous H(2)S and its relation to antioxidation and down-regulation of c-fos mRNA were investigated in the present

A critical role for cystathionine-β-synthase in hydrogen sulfide-mediated hypoxic relaxation of the coronary artery.

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Hypoxia-induced coronary artery vasodilatation protects the heart by increasing blood flow under ischemic conditions, however its mechanism is not fully elucidated. Hydrogen sulfide (H2S) is reported to be an oxygen sensor/transducer in the vasculature. The present study aimed to identify and

Mild neonatal hypoxia exacerbates the effects of vitamin-deficient diet on homocysteine metabolism in rats.

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Elevated plasma homocysteine has been linked to pregnancy complications and developmental diseases. Whereas hyperhomocysteinemia is frequently observed in populations at risk of malnutrition, hypoxia may alter the remethylation of homocysteine in hepatocytes. We aimed to investigate the combined

Influence of preconditioning-like hypoxia on the liver of developing methyl-deficient rats.

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Deficiency in nutritional determinants of homocysteine (HCY) metabolism, such as vitamin B(12) and folate, during pregnancy is known to influence HCY levels in the progeny, which in turn may exert adverse effects during development, including liver defects. Since short hypoxia has been shown to

Blood-brain amino acid transport and content during anoxia and reoxygenation.

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The isolated dog brain preparation was used to investigate the dynamics of cerebral amino acid metabolism during perfusion with anoxic blood (PO2 less than 10 mmHg). Significant uptake of histidine and lysine, as determined by arteriovenous (A-V) differences in whole blood samples, was observed

Association of Cystathionine β-Synthase Gene Polymorphisms With Preeclampsia.

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Preeclampsia (PE) is a pregnancy disorder that increases maternal and fetal morbidity and mortality worldwide. High plasma levels of homocysteine (Hcy) are a risk factor for several cardiovascular diseases. Cystathionine β-synthase (CBS) plays an important role in Hcy homeostasis catalyzing the

Transcriptional Induction of Cystathionine γ-Lyase, a Reactive Sulfur-Producing Enzyme, by Copper Diethyldithiocarbamate in Cultured Vascular Endothelial Cells

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As toxic substances can enter the circulating blood and cross endothelial monolayers to reach parenchymal cells in organs, vascular endothelial cells are an important target compartment for such substances. Reactive sulfur species protect cells against oxidative stress and toxic substances,

Cystathionine gamma-lyase-deficient smooth muscle cells exhibit redox imbalance and apoptosis under hypoxic stress conditions.

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BACKGROUND Hydrogen sulphide (H(2)S) has recently emerged as a novel and important gasotransmitter in the cardiovascular system, where it is generated mainly by cystathionine gamma-lyase (CSE). Abnormal metabolism and functions of the CSE/H(2)S pathway have been linked to various cardiovascular

DL-Propargylglycine protects against myocardial injury induced by chronic intermittent hypoxia through inhibition of endoplasmic reticulum stress.

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BACKGROUND Chronic intermittent hypoxia (CIH), an important basis of the pathogenesis of organ damage induced by obstructive sleep apnea syndrome (OSAS), is associated with myocardial injury, such as left ventricular dysfunction, apoptosis, and oxidative stress. Endogenous hydrogen sulfide (H2S)
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