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. 2016 Feb;11(2):226-7.
doi: 10.4103/1673-5374.177720.

Consequences of hepatic damage after traumatic brain injury: current outlook and potential therapeutic targets

Sonia Villapol  1
Affiliations

Consequences of hepatic damage after traumatic brain injury: current outlook and potential therapeutic targets

Sonia Villapol. Neural Regen Res. 2016 Feb.
No abstract available

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Figures

Figure 1
Figure 1
Brain-liver communication. (A) The interplay between the brain and liver after traumatic brain injury (TBI). TBI induces central and peripheral inflammation and triggers the induction of acute phase response. Serum amyloid A1 (SAA1) is produced and secreted by the damaged liver. The inhibition of SAA1 using pharmacological or oligonucleotides therapies could abolish neurotoxicity in the brain. (B) SAA1 receptors and signaling pathways. SAA1 can bind the receptors RAGE (receptor for advanced glycation end-products), FPRL1 (formyl peptide receptor-like 1), CD36 (cluster of differentiation 36), or TLR2/4 (Toll-like receptors 2 or 4). SAA1 induces the activation of ERK (extracellular signal-regulated kinase) and JNK (c-Jun N-terminal kinase)/p38 signaling pathways activating the transcription factors NF-kB (nuclear factor kappa B), AP-1 (activating protein 1) or the SAA-activating factor 1 (SAF-1) that induces the production of SAA1. Consequently, SAA1 stimulates the expression of MCP-1 (monocyte chemoattractant protein 1), MMP (matrix metalloproteinase), NOS (nitric oxide synthetase), M-CSF (macrophage colony-stimulating factor), ROS (reactive oxygen species), COX-2 (cyclooxygenase-2) or pro-inflammatory cytokines. Alternatively, SAA1 synthesis can be induced by TNFα (tumor necrosis factor-alpha), IL-1β or IL-6.
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