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10.14800/ics.111 http://scihub22266oqcxt.onion/10.14800/ics.111 C4457460!4457460!26052540     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Inflamm+Cell+Signal 2014 ; 1 (3): ä Nephropedia Template TP {{tp|p=26052540|t=2014. Novel Therapeutic Targets in Neuroinflammation and Neuropathic Pain |pdf=|usr=}}{{26052540}} gab.com Text Novel Therapeutic Targets in Neuroinflammation and Neuropathic Pain JO: Inflamm Cell Signal http://www.kidney.de/pget.php?&tw=1&pmid=26052540 #FOAvip There is abounding evidence that neuroinflammation plays a major role in the pathogenesis of neurodegeneration and neuropathic pain. Chemokine-induced recruitment of peripheral immune cells is a central feature in inflammatory neurodegenerative disorders. Immune cells, glial cells and neurons constitute an integral network that coordinates the immune response by releasing inflammatory mediators that in turn modulate inflammation, neurodegeneration and the signal transduction of pain, via interaction with neurotransmitters and their receptors. The chemokine monocyte chemoattractant protein-1/ chemokine (C-C motif) ligand (MCP-1/CCL2) and its receptor C-C chemokine receptor (CCR2) play a major role in mediating neuroinflammation and targeting CCL2/CCR2 represents a promising strategy to limit neuroinflammation-induced neuropathy. In addition, the CCL2/CCR2 axis is also involved in mediating the pain response. Key cellular signaling events such as phosphorylation and subsequent activation of mitogen activated protein kinase (MAPK) p38 and its substrate MAPK-activated protein MAPKAP Kinase (MK) MK-2, regulate neuroinflammation, neuronal survival and synaptic activity. Further, MAPKs such as extracellular signal-regulated kinases (ERK), c-jun N-terminal kinase (JNK) and p38 play vital roles in mediating the pain signaling cascade and contribute to the maintenance of peripheral and central neuronal sensitization associated with chronic pain. This review outlines the rationale for developing therapeutic strategies against CCL2/CCR2 and MAPK signaling networks, identifying them as novel therapeutic targets for limiting neuroinflammation and neuropathic pain. Twit Text FOAVip Novel Therapeutic Targets in Neuroinflammation and Neuropathic Pain ????Inflamm Cell Signal http://www.kidney.de/pget.php?&tw=1&pmid=26052540 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26052540 #FOAvip English Wikipedia <ref>{{Cite pmid|26052540}}</ref> Novel Therapeutic Targets in Neuroinflammation and Neuropathic Pain #MMPMID26052540 Ramesh G Inflamm Cell Signal 2014[]; 1 (3): ä PMID26052540show ga There is abounding evidence that neuroinflammation plays a major role in the pathogenesis of neurodegeneration and neuropathic pain. Chemokine-induced recruitment of peripheral immune cells is a central feature in inflammatory neurodegenerative disorders. Immune cells, glial cells and neurons constitute an integral network that coordinates the immune response by releasing inflammatory mediators that in turn modulate inflammation, neurodegeneration and the signal transduction of pain, via interaction with neurotransmitters and their receptors. The chemokine monocyte chemoattractant protein-1/ chemokine (C-C motif) ligand (MCP-1/CCL2) and its receptor C-C chemokine receptor (CCR2) play a major role in mediating neuroinflammation and targeting CCL2/CCR2 represents a promising strategy to limit neuroinflammation-induced neuropathy. In addition, the CCL2/CCR2 axis is also involved in mediating the pain response. Key cellular signaling events such as phosphorylation and subsequent activation of mitogen activated protein kinase (MAPK) p38 and its substrate MAPK-activated protein MAPKAP Kinase (MK) MK-2, regulate neuroinflammation, neuronal survival and synaptic activity. Further, MAPKs such as extracellular signal-regulated kinases (ERK), c-jun N-terminal kinase (JNK) and p38 play vital roles in mediating the pain signaling cascade and contribute to the maintenance of peripheral and central neuronal sensitization associated with chronic pain. This review outlines the rationale for developing therapeutic strategies against CCL2/CCR2 and MAPK signaling networks, identifying them as novel therapeutic targets for limiting neuroinflammation and neuropathic pain. äNovel Therapeutic Targets in Neuroinflammation and Neuropathic Pain (epmc).pdf DeepDyve Pubget Overpricing