Cigarette smoke extract induces endothelial cell injury via JNK pathway
Biochemical and Biophysical Research Communications, ISSN: 0006-291X, Vol: 329, Issue: 1, Page: 58-63
2005
- 67Citations
- 27Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations67
- Citation Indexes67
- 67
- CrossRef49
- Captures27
- Readers27
- 27
Article Description
Cigarette smoking is the most crucial factor responsible for chronic obstructive pulmonary disease (COPD). The precise mechanisms of the development of the disease have, however, not been fully understood. Recently, impairment of pulmonary endothelial cells has been increasingly recognized as a critical pathophysiological process in COPD. To verify this hypothesis, we examined how cigarette smoke extract (CSE) damages human umbilical vein endothelial cells (HUVECs). CSE activated c-Jun N-terminal kinase (JNK), and treatment of HUVECs with SP600125, a specific inhibitor of the JNK pathway, significantly suppressed endothelial cell damage by CSE. In contrast, inhibition of the extracellular-regulated kinase or the p38 pathway did not affect the cytotoxicity of CSE. Furthermore, anti-oxidants superoxide dismutase and catalase reduced CSE-induced JNK phosphorylation and endothelial cell injury. These results indicate that CSE damages vascular endothelial cells through the JNK pathway activated, at least partially, by oxidative stress.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006291X05001531; http://dx.doi.org/10.1016/j.bbrc.2005.01.095; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=13844255721&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/15721273; https://linkinghub.elsevier.com/retrieve/pii/S0006291X05001531; https://dx.doi.org/10.1016/j.bbrc.2005.01.095
Elsevier BV
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