Nicotine stimulates angiogenesis and promotes tumor growth and atherosclerosis
By C. Heeschen, James J. Jang, M. Weis, Anjali Pathak, S. Kaji, Robert S. Hu, P. Tsao, Frances L. Johnson, J. Cooke. Nature Medicine, 2001
798 citations recorded by the source corpus.
Subfields: Molecular Biology, Psychiatry and Mental health
View Paper: https://www.semanticscholar.org/paper/9b37ef0b39e0793a3453433d342abd8898386939
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In Molecular Biology
Citations in the corpus
- iArc monogrAphs on the evAluAtion oF cArcinogenic risks to humAns (2012, background): “This can cause decreased apoptosis, increased angiogen esis, and increased transformation (Heeschen et al., 2001; West et al., 2003).”
- Neuronal nicotinic receptors: from structure to pathology. (2004, background): “Nic is a potent stimulus of angiogenesis and increases proliferation in endothelial cells acting through NAChRs (Heeschen et al., 2001; Villablanca, 1998).”
- Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. (2003, neutral): “For example, nicotine has been shown to have proangiogenic properties by inducing endogenous VEGF (43).”
- The alpha7 nicotinic acetylcholine receptor as a pharmacological target for inflammation (2007, background): “Consistent with these results, COX-2- and PKA inhibitors prevent the effects of nicotine on adhesion molecule expression and cytokine production, indicating that the mechanism of action of nicotine may be via endogenous PGE2 production (Heeschen et al., 2001; Takahashi et al., 2006).”