The DOI matches its Crossref record; 40 of the 40 references it cites were found in a registry or an index.
Nicotine promotes atherosclerosis via ROS-NLRP3-mediated endothelial cell pyroptosis
Open accessAbstract
Cigarette smoking is a major risk factor for atherosclerosis and other cardiovascular diseases. Increasing evidence has demonstrated that nicotine impairs the cardiovascular system by targeting vascular endothelial cells, but the underlying mechanisms remain obscure. It is known that cell death and inflammation are crucial processes leading to atherosclerosis. We proposed that pyroptosis may be implicated in nicotine-induced atherosclerosis and therefore conducted the present study. We found that nicotine resulted in larger atherosclerotic plaques and secretion of inflammatory cytokines in ApoE−/− mice fed with a high-fat diet (HFD). Treatment of human aortic endothelial cells (HAECs) with nicotine resulted in NLRP3-ASC inflammasome activation and pyroptosis, as evidenced by cleavage of caspase-1, production of downstream interleukin (IL)-1β and IL-18, and elevation of LDH activity and increase of propidium iodide (PI) positive cells, which were all inhibited by caspase-1 inhibitor. Moreover, silencing NLRP3 or ASC by small interfering RNA efficiently suppressed nicotine-induced caspase-1 cleavage, IL-18 and IL-1β production, and pyroptosis in HAECs. Further experiments revealed that the nicotine-NLRP3-ASC-pyroptosis pathway was activated by reactive oxygen species (ROS), since ROS scavenger (N-acetyl-cysteine, NAC) prevented endothelial cell pyroptosis. We conclude that pyroptosis is likely a cellular mechanism for the pro-atherosclerotic property of nicotine and stimulation of ROS to activate NLRP3 inflammasome is a signaling mechanism for nicotine-induced pyroptosis.
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Cites
Schroder, K., & Tschopp, J. (2010) · Cell · doi:10.1016/j.cell.2010.01.040 · Cited by 5,475
Lusis, A. J. (2000) · Nature · doi:10.1038/35025203 · Cited by 4,839
NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
Duewell, P., Kono, H., Rayner, K. J., Sirois, C. M., Vladimer, G., Bauernfeind, F. G., Abela, G. S., Franchi, L., Nuñez, G., Schnurr, M., et al. (2010) · Nature · doi:10.1038/nature08938 · Cited by 4,026
The pathophysiology of cigarette smoking and cardiovascular disease
Ambrose, J. A., & Barua, R. S. (2004) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2003.12.047 · Cited by 2,394
Franchi, L., Eigenbrod, T., Muñoz-Planillo, R., & Nuñez, G. (2009) · Nature Immunology · doi:10.1038/ni.1703 · Cited by 1,834
Caspase-1-induced pyroptosis is an innate immune effector mechanism against intracellular bacteria
Miao, E. A., Leaf, I. A., Treuting, P. M., Mao, D. P., Dors, M., Sarkar, A., Warren, S. E., Wewers, M. D., & Aderem, A. (2010) · Nature Immunology · doi:10.1038/ni.1960 · Cited by 1,336
Hemodynamic shear stress and the endothelium in cardiovascular pathophysiology
Davies, P. F. (2009) · Nature Clinical Practice Cardiovascular Medicine · doi:10.1038/ncpcardio1397 · Cited by 1,209
Caspase‐1‐induced pyroptotic cell death
Miao, E. A., Rajan, J. V., & Aderem, A. (2011) · Immunological Reviews · doi:10.1111/j.1600-065x.2011.01044.x · Cited by 1,137
Wree, A., Eguchi, A., McGeough, M. D., Pena, C. A., Johnson, C. D., Canbay, A., Hoffman, H. M., & Feldstein, A. E. (2014) · Hepatology · doi:10.1002/hep.26592 · Cited by 945
Nicotine stimulates angiogenesis and promotes tumor growth and atherosclerosis
Heeschen, C., Jang, J. J., Weis, M., Pathak, A., Kaji, S., Hu, R. S., Tsao, P. S., Johnson, F. L., & Cooke, J. P. (2001) · Nature Medicine · doi:10.1038/89961 · Cited by 800
Cited by
The NLRP3 inflammasome: contributions to inflammation-related diseases
Chen, Y., Ye, X., Escames, G., Lei, W., Zhang, X., Li, M., Jing, T., Yao, Y., Qiu, Z., Wang, Z., et al. (2023) · Cellular & Molecular Biology Letters · doi:10.1186/s11658-023-00462-9 · Cited by 492
Zeng, C., Duan, F., Hu, J., Luo, B., Huang, B., Lou, X., Sun, X., Li, H., Zhang, X., Yin, S., et al. (2020) · Redox Biology · doi:10.1016/j.redox.2020.101523 · Cited by 384
Yan, H., Luo, B., Wu, X., Guan, F., Yu, X., Zhao, L., Ke, X., Wu, J., & Yuan, J. (2021) · International Journal of Biological Sciences · doi:10.7150/ijbs.60292 · Cited by 303
Self-citationRole of pyroptosis in cardiovascular diseases
Jia, C., Chen, H., Zhang, J., Zhou, K., Zhuge, Y., Niu, C., Qiu, J., Rong, X., Shi, Z., Xiao, J., et al. (2019) · International Immunopharmacology · doi:10.1016/j.intimp.2018.12.028 · Cited by 267
New mechanism of nerve injury in Alzheimer’s disease: β‐amyloid‐induced neuronal pyroptosis
Han, C., Yang, Y., Guan, Q., Zhang, X., Shen, H., Sheng, Y., Wang, J., Zhou, X., Li, W., Guo, L., et al. (2020) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.15439 · Cited by 193
Metadata
- Authors
- Wu, X., Zhang, H., Qi, W., Zhang, Y., Li, J., Li, Z., Lin, Y., Bai, X., Liu, X., Chen, X., Yang, H., Xu, C., Zhang, Y., & Yang, B.
- Venue
- Cell Death & Disease
- Published
- 2018-02-07
- Volume
- 9
- Issue
- 2
- Pages
- 171-171
- ISSN
- 2041-4889 (ISSN-L)
- OpenAlex
- W2789997601
- Cited by
- 586
- References
- 40
- FWCI
- 14.60
- Type
- journal article
- Language
- en
- Open access
- gold
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- Wu, X., Zhang, H., Qi, W., Zhang, Y., Li, J., Li, Z., Lin, Y., Bai, X., Liu, X., Chen, X., Yang, H., Xu, C., Zhang, Y., & Yang, B. (2018). Nicotine promotes atherosclerosis via ROS-NLRP3-mediated endothelial cell pyroptosis. Cell Death & Disease. https://doi.org/10.1038/s41419-017-0257-3
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