Protein steady-state levels of S-adenosylhomocysteine-hydrolase and cystathionine gamma-lyase diminished but methylthioadenosine phosphorylase levels increased in pancreas with acute pancreatitis.
In a proteomic screen, we identified cystathionine γ-lyase (CTH) as a marker for clear cell carcinoma, as it is expressed at high levels in clear cell carcinomas of the ovary and endometrium.
We used mice genetically deficient in the cystathionine γ-lyase enzyme (CSE), the major H<sub>2</sub>S-generating enzyme in the lung to determine the contribution of H<sub>2</sub>S to airway disease in response to side-stream tobacco smoke (TS), and to TS/RSV co-exposure.
The aim of the present study is to examine whether the age-dependent development of allergic asthma is caused by age-dependent expression of cystathionine gamma-lyase (CSE), a key enzyme that catalyzes the production of hydrogen sulfide (H<sub>2</sub>S).
Lowering endogenous production of H<sub>2</sub> S by concomitant silencing of cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS) favoured VIC calcification. analysis of human specimens revealed higher Expression of CSE in aorta stenosis valves with calcification (AS) was higher than in valves of aortic insufficiency (AI).
Lowering endogenous production of H<sub>2</sub> S by concomitant silencing of cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS) favoured VIC calcification. analysis of human specimens revealed higher Expression of CSE in aorta stenosis valves with calcification (AS) was higher than in valves of aortic insufficiency (AI).
Blocking the CB hyperactivity with L-propargylglycine, an inhibitor of cystathionine-γ-lyase (CSE), which catalyzes H<sub>2</sub>S synthesis, prevented apneas in HO-2<sup>-/-</sup> mice.
Cystathionine γ lyase (CSE) is the major source of hydrogen sulfide-derived species (H<sub>2</sub>S<sub>n</sub>) in endothelial cells and plays an important role in protecting against atherosclerosis.
Therefore, we aimed to evaluate the involvement of hydrogen sulfide (H <sub>2</sub> S)/cystathionine γ-lyase (CSE) in the pathogenesis of AS as well as their possible signaling pathways.
Inhibition of HDAC6 activity may improve endothelial function and prevent or reverse the development of atherosclerosis.<b>NEW & NOTEWORTHY</b> Oxidative injury to endothelial cells by oxidized LDL reduced cystathionine γ-lyase (CSEγ) expression and H<sub>2</sub>S production, leading to endothelial dysfunction, which was prevented by histone deacetylase 6 (HDAC6) inhibition.
The present study investigated the effect of cystathionine on astrocytoma (U373) cell proliferation, the activity of γ-cystathionase (CTH) and changes in thiols levels.
Inhibition of HDAC6 activity may improve endothelial function and prevent or reverse the development of atherosclerosis.<b>NEW & NOTEWORTHY</b> Oxidative injury to endothelial cells by oxidized LDL reduced cystathionine γ-lyase (CSEγ) expression and H<sub>2</sub>S production, leading to endothelial dysfunction, which was prevented by histone deacetylase 6 (HDAC6) inhibition.
Therefore, we aimed to evaluate the involvement of hydrogen sulfide (H <sub>2</sub> S)/cystathionine γ-lyase (CSE) in the pathogenesis of AS as well as their possible signaling pathways.
Cystathionine γ lyase (CSE) is the major source of hydrogen sulfide-derived species (H<sub>2</sub>S<sub>n</sub>) in endothelial cells and plays an important role in protecting against atherosclerosis.
This study provides new insights into the interaction of H<sub>2</sub>S and estrogen signaling pathways on the regulation of cardiovascular functions.<b>NEW & NOTEWORTHY</b> Female cystathionine γ-lyase (CSE)-knockout mice have significantly lower plasma estrogen levels and more severe early atherosclerotic lesion than female wild-type mice.
Additional work is needed to comprehensively evaluate genomic variation in CTH and related genes in the trans-sulfuration pathway and bladder cancer risk.
The enhanced Ca<sub>v</sub>3.2 activity by H<sub>2</sub>S formed by the upregulated cystathionine-γ-lyase (CSE) is involved in the cyclophosphamide (CPA)-induced cystitis-related bladder pain in mice.
Involvement of the cystathionine-γ-lyase/Ca<sub>v</sub>3.2 pathway in substance P-induced bladder pain in the mouse, a model for nonulcerative bladder pain syndrome.
Cystathionine γ-lyase (CSE) is highly expressed in breast cancer, and can promote breast cancer development and progression; therefore, inhibitors of CSE may be of great significance for the treatment of breast cancer.