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10.1016/j.cmet.2014.07.011 http://scihub22266oqcxt.onion/10.1016/j.cmet.2014.07.011 C4156549!4156549 !25130399     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25130399 &cmd=llinks): Failed to open stream: HTTP request failed! 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Mitochondrial complex I activity suppresses inflammation and enhances bone resorption by shifting macrophage-osteoclast polarization |pdf=|usr=}}{{25130399 }} gab.com Text Mitochondrial complex I activity suppresses inflammation and enhances bone resorption by shifting macrophage-osteoclast polarization JO: Cell Metab http://www.kidney.de/pget.php?&tw=1&pmid=25130399 #FOAvip Mitochondrial complex I (CI) deficiency is associated with multiple neurological and metabolic disorders. However, its effect on innate immunity and bone remodeling is unclear. Using deletion of the essential CI subunit Ndufs4 as a model for mitochondrial dysfunction, we report that mitochondria suppress macrophage activation and inflammation while promoting osteoclast differentiation and bone resorption via both cell-autonomous and systemic regulation. Global Ndufs4 deletion causes systemic inflammation and osteopetrosis. Hematopoietic Ndufs4 deletion causes an intrinsic lineage shift from osteoclast to macrophage. Liver Ndufs4 deletion causes a metabolic shift from fatty acid oxidation to glycolysis, accumulating fatty acids and lactate (FA/LAC) in the circulation. FA/LAC further activates Ndufs4(-/-) macrophages via reactive oxygen species induction and diminishes osteoclast lineage commitment in Ndufs4(-/-) progenitors; both inflammation and osteopetrosis in Ndufs4(-/-) mice are attenuated by TLR4/2 deletion. Together, these findings reveal mitochondrial CI as a critical rheostat of innate immunity and skeletal homeostasis. Twit Text FOAVip Mitochondrial complex I activity suppresses inflammation and enhances bone resorption by shifting macrophage-osteoclast polarization ????Cell Metab http://www.kidney.de/pget.php?&tw=1&pmid=25130399 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25130399 #FOAvip English Wikipedia <ref>{{Cite pmid|25130399 }}</ref> Mitochondrial complex I activity suppresses inflammation and enhances bone resorption by shifting macrophage-osteoclast polarization #MMPMID25130399 Jin Z ; Wei W ; Yang M ; Du Y ; Wan Y Cell Metab 2014[Sep]; 20 (3 ): 483-98 PMID25130399 show ga Mitochondrial complex I (CI) deficiency is associated with multiple neurological and metabolic disorders. However, its effect on innate immunity and bone remodeling is unclear. Using deletion of the essential CI subunit Ndufs4 as a model for mitochondrial dysfunction, we report that mitochondria suppress macrophage activation and inflammation while promoting osteoclast differentiation and bone resorption via both cell-autonomous and systemic regulation. Global Ndufs4 deletion causes systemic inflammation and osteopetrosis. Hematopoietic Ndufs4 deletion causes an intrinsic lineage shift from osteoclast to macrophage. Liver Ndufs4 deletion causes a metabolic shift from fatty acid oxidation to glycolysis, accumulating fatty acids and lactate (FA/LAC) in the circulation. FA/LAC further activates Ndufs4(-/-) macrophages via reactive oxygen species induction and diminishes osteoclast lineage commitment in Ndufs4(-/-) progenitors; both inflammation and osteopetrosis in Ndufs4(-/-) mice are attenuated by TLR4/2 deletion. Together, these findings reveal mitochondrial CI as a critical rheostat of innate immunity and skeletal homeostasis. |Alopecia/complications/genetics/immunology/pathology [MESH] |Animals [MESH] |Bone Resorption/*complications/genetics/*immunology/pathology [MESH] |Cell Differentiation [MESH] |Electron Transport Complex I/*deficiency/genetics/immunology [MESH] |Fatty Acids/metabolism [MESH] |Female [MESH] |Gene Deletion [MESH] |Glycolysis [MESH] |Immunity, Innate [MESH] |Macrophage Activation [MESH] |Macrophages/immunology/*pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mitochondria/immunology/pathology [MESH] |Mitochondrial Diseases/*complications/genetics/*immunology/pathology [MESH] |Osteoclasts/cytology/immunology/*pathology [MESH]Mitochondrial complex I activity suppresses inflammation and enhances (epmc).pdf DeepDyve Pubget Overpricing