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. Author manuscript; available in PMC: 2017 Mar 23.
Published in final edited form as: Med Hypotheses. 2014 Jan 14;83(6):640–643. doi: 10.1016/j.mehy.2013.12.027

Figure 1.

Figure 1

Hypothetical scheme in which MyD88 plays an essential role in NFκB-related gene products, which results in endothelial dysfunction and vascular hypertrophy in Ang II-dependent hypertension. Ang II increases TLR4 expression, however the mechanism of which is not clear. In addition, the AT1 receptor via Ang II increases NFκB activation.