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. 2016 Sep 23;14:276. doi: 10.1186/s12967-016-1032-4

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© The Author(s) 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 6 — Summary of pathways by leptin on PCSK9 and LDLR expression in HepG2 cells. Stimulation of p38MAPK pathway by leptin increased expression of nuclear HNF1α which could bind to PCSK9 promoter, leading to increase PCSK9 expression in HepG2 cells. The increased PCSK9 leaded to elevated LDLR degradation and inhibited LDL uptake