The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
The hydrogen sulfide donor, GYY 4137, exhibits anti‐atherosclerotic activity in high fat fed apolipoprotein E−/− mice
Open accessAbstract
Background and Purpose: Atherosclerosis is associated with reduced vascular hydrogen sulfide (H 2 S) biosynthesis. GYY4137 is a novel slow‐releasing H 2 S compound that may effectively mimic the time course of H 2 S release in vivo. However, it is not known whether GYY4137 affects atherosclerosis. Experimental Approach: RAW 264.7 cells and human blood monocyte‐derived macrophages were incubated with oxidized low density lipoprotein (ox‐LDL) with/without GYY4137. ApoE−/− mice were fed a high‐fat diet for 4 weeks and administered GYY4137 for 30 days. Lipid and atherosclerotic lesions were measured by oil red O staining. Endothelium‐dependent relaxation was assessed in response to acetylcholine. Superoxide production was detected by dihydroethidium staining. Expression of mRNA and protein were evaluated by quantitative real‐time PCR and Western blot. Key Results: GYY4137 inhibited ox‐LDL‐induced foam cell formation and cholesterol esterification in cultured cells. GYY4137 decreased the expression of lectin‐like ox‐LDL receptor‐1, iNOS, phosphorylated IκBα, NF‐κB, ICAM‐1, VCAM‐1 and chemokines, including CXCL 2, CXCR4, CXCL 10 and CCL 17, but increased the scavenger protein CD36, in ox‐LDL‐treated RAW 264.7 cells. In vivo, GYY4137 decreased aortic atherosclerotic plaque formation and partially restored aortic endothelium‐dependent relaxation in apoE−/− mice. GYY4137 decreased ICAM‐1, TNF‐α and IL‐6 mRNA expression as well as superoxide (O 2−) generation in aorta. In addition, GYY4137 increased aortic eNOS phosphorylation and expression of PI3K, enhanced A kt Ser 473 phosphorylation and down‐regulated the expression of LOX‐1. Conclusion and Implications: GYY4137 inhibits lipid accumulation induced by ox‐LDL in RAW 264.7 cells. In vivo, GYY4137 decreased vascular inflammation and oxidative stress, improved endothelial function and reduced atherosclerotic plaque formation in apo E−/− mice.
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Cites
Inflammation in atherosclerosis
Libby, P. (2002) · Nature · doi:10.1038/nature01323 · Cited by 8,315
Animal research: Reporting in vivo experiments: The ARRIVE guidelines
Kilkenny, C., Browne, W., Cuthill, I. C., Emerson, M., & Altman, D. G. (2010) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2010.00872.x · Cited by 3,625
Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation
Dimmeler, S., Fleming, I., Fisslthaler, B., Hermann, C., Busse, R., & Zeiher, A. M. (1999) · Nature · doi:10.1038/21224 · Cited by 3,591
Role of Endothelial Dysfunction in Atherosclerosis
Davignon, J., & Ganz, P. (2004) · Circulation · doi:10.1161/01.cir.0000131515.03336.f8 · Cited by 2,513
H 2 S as a Physiologic Vasorelaxant: Hypertension in Mice with Deletion of Cystathionine γ-Lyase
Yang, G., Wu, L., Jiang, B., Yang, W., Qi, J., Cao, K., Meng, Q., Mustafa, A. K., Mu, W., Zhang, S., et al. (2008) · Science · doi:10.1126/science.1162667 · Cited by 2,310
Guide to receptors and channels (GRAC), 5th edition
Alexander, S., Mathie, A., & Peters, J. (2011) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2011.01649_1.x · Cited by 1,947
Guidelines for reporting experiments involving animals: the ARRIVE guidelines
McGrath, J., Drummond, G., McLachlan, E., Kilkenny, C., & Wainwright, C. (2010) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2010.00873.x · Cited by 1,592
Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology
Li, J.-M., & Shah, A. M. (2004) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00124.2004 · Cited by 773
Wang, Y., Zhao, X., Jin, H., Wei, H., Li, W., Bu, D., Tang, X., Ren, Y., Tang, C., & Du, J. (2009) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.108.179333 · Cited by 307
Vita, J. A. (2011) · Circulation · doi:10.1161/circulationaha.111.078824 · Cited by 195
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Chemical Biology of H2S Signaling through Persulfidation
Filipovic, M. R., Zivanovic, J., Alvarez, B., & Banerjee, R. (2018) · Chemical Reviews · doi:10.1021/acs.chemrev.7b00205 · Cited by 1,046
Sun, H.-J., Wu, Z.-Y., Nie, X.-W., & Bian, J.-S. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2019.01568 · Cited by 554
Szabo, C., & Papapetropoulos, A. (2017) · Pharmacological Reviews · doi:10.1124/pr.117.014050 · Cited by 423
The Contribution of Homocysteine Metabolism Disruption to Endothelial Dysfunction: State-of-the-Art
Esse, R., Barroso, M., Tavares de Almeida, I., & Castro, R. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20040867 · Cited by 336
The CXCL12/CXCR4 chemokine ligand/receptor axis in cardiovascular disease
Döring, Y., Pawig, L., Weber, C., & Noels, H. (2014) · Frontiers in Physiology · doi:10.3389/fphys.2014.00212 · Cited by 289
Hu, H., Shao, W., Liu, Q., Liu, N., Wang, Q., Xu, J., Zhang, X., Weng, Z., Lu, Q., Jiao, L., et al. (2022) · Nature Communications · doi:10.1038/s41467-021-27758-8 · Cited by 283
Hydrogen sulfide in physiology and diseases of the digestive tract
Singh, S., & Lin, H. (2015) · Microorganisms · doi:10.3390/microorganisms3040866 · Cited by 260
Hydrogen Sulfide and Endothelial Dysfunction: Relationship with Nitric Oxide
Altaany, Z., Moccia, F., Munaron, L., Mancardi, D., & Wang, R. (2014) · Current Medicinal Chemistry · doi:10.2174/0929867321666140706142930 · Cited by 86
Zhao, H., Yan, R., Zhou, X., Ji, F., & Zhang, B. (2016) · International Immunopharmacology · doi:10.1016/j.intimp.2016.07.020 · Cited by 61
Metadata
- Authors
- Liu, Z., Han, Y., Li, L., Lu, H., Meng, G., Li, X., Shirhan, M., Peh, M. T., Xie, L., Zhou, S., Wang, X., Chen, Q., Dai, W., Tan, C., Pan, S., Moore, P. K., & Ji, Y.
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 2013-07-26
- Volume
- 169
- Issue
- 8
- Pages
- 1795-1809
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- OpenAlex
- W1526236056
- Cited by
- 181
- References
- 10
- FWCI
- 7.24
- Type
- journal article
- Language
- en
- Open access
- green
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