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10.15252/emmm.201607492 http://scihub22266oqcxt.onion/10.15252/emmm.201607492 C5582411!5582411!28674080     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+Mol+Med 2017 ; 9 (9): 1244-62 Nephropedia Template TP {{tp|p=28674080|t=2017. Macrophage deficiency of miR?21 promotes apoptosis, plaque necrosis, and vascular inflammation during atherogenesis |pdf=|usr=}}{{28674080}} gab.com Text Macrophage deficiency of miR 21 promotes apoptosis, plaque necrosis, and vascular inflammation during atherogenesis JO: EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=28674080 #FOAvip Atherosclerosis, the major cause of cardiovascular disease, is a chronic inflammatory disease characterized by the accumulation of lipids and inflammatory cells in the artery wall. Aberrant expression of microRNAs has been implicated in the pathophysiological processes underlying the progression of atherosclerosis. Here, we define the contribution of miR?21 in hematopoietic cells during atherogenesis. Interestingly, we found that miR?21 is the most abundant miRNA in macrophages and its absence results in accelerated atherosclerosis, plaque necrosis, and vascular inflammation. miR?21 expression influences foam cell formation, sensitivity to ER?stress?induced apoptosis, and phagocytic clearance capacity. Mechanistically, we discovered that the absence of miR?21 in macrophages increases the expression of the miR?21 target gene, MKK3, promoting the induction of p38?CHOP and JNK signaling. Both pathways enhance macrophage apoptosis and promote the post?translational degradation of ABCG1, a transporter that regulates cholesterol efflux in macrophages. Altogether, these findings reveal a major role for hematopoietic miR?21 in atherogenesis. Twit Text FOAVip Macrophage deficiency of miR 21 promotes apoptosis, plaque necrosis, and vascular inflammation during atherogenesis ????EMBO Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=28674080 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28674080 #FOAvip English Wikipedia <ref>{{Cite pmid|28674080}}</ref> Macrophage deficiency of miR?21 promotes apoptosis, plaque necrosis, and vascular inflammation during atherogenesis #MMPMID28674080 Canfrán?Duque A; Rotllan N; Zhang X; Fernández?Fuertes M; Ramírez?Hidalgo C; Araldi E; Daimiel L; Busto R; Fernández?Hernando C; Suárez Y EMBO Mol Med 2017[Sep]; 9 (9): 1244-62 PMID28674080show ga Atherosclerosis, the major cause of cardiovascular disease, is a chronic inflammatory disease characterized by the accumulation of lipids and inflammatory cells in the artery wall. Aberrant expression of microRNAs has been implicated in the pathophysiological processes underlying the progression of atherosclerosis. Here, we define the contribution of miR?21 in hematopoietic cells during atherogenesis. Interestingly, we found that miR?21 is the most abundant miRNA in macrophages and its absence results in accelerated atherosclerosis, plaque necrosis, and vascular inflammation. miR?21 expression influences foam cell formation, sensitivity to ER?stress?induced apoptosis, and phagocytic clearance capacity. Mechanistically, we discovered that the absence of miR?21 in macrophages increases the expression of the miR?21 target gene, MKK3, promoting the induction of p38?CHOP and JNK signaling. Both pathways enhance macrophage apoptosis and promote the post?translational degradation of ABCG1, a transporter that regulates cholesterol efflux in macrophages. Altogether, these findings reveal a major role for hematopoietic miR?21 in atherogenesis. äMacrophage deficiency of miR?21 promotes apoptosis, plaque necrosis, a(epmc).pdf DeepDyve Pubget Overpricing