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10.18632/oncotarget.25173 http://scihub22266oqcxt.onion/10.18632/oncotarget.25173 C5955156!5955156!29774121     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2018 ; 9 (31): 22047-57 Nephropedia Template TP {{tp|p=29774121|t=2018. MiR-33 promotes myocardial fibrosis by inhibiting MMP16 and stimulating p38 MAPK signaling |pdf=|usr=}}{{29774121}} gab.com Text MiR-33 promotes myocardial fibrosis by inhibiting MMP16 and stimulating p38 MAPK signaling JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=29774121 #FOAvip Myocardial fibrosis occurs in the late stages of many cardiovascular diseases, and appears to be stimulated by various microRNAs (miRNAs). We previously found that miR-33 may stimulate cardiac remodeling. Here, we examined the involvement of miR-33 in myocardial fibrosis. Proximal left coronary descending artery occlusion was performed in rat, and antagomiR-33a was injected. Primary cardiac fibroblasts were cultured and transfected with miR-33a mimics and inhibitors. miR-33a levels were increased in the rat after surgery, and collagen deposition and heart fibrosis were observed in vivo. Inhibition of miR-33a suppressed fibroblast proliferation, reduced the mRNA and protein levels of collagen-related markers in vitro and in vivo, and rescued the histological damage in vivo. A dual-luciferase reporter system showed that matrix metalloproteinase 16 (MMP16) gene was the direct target of MiR-33a. These results suggest that miR-33 promoted myocardial fibrosis by inhibiting MMP16 and stimulating p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway. MiR-33 may act as a novel therapeutic target for treating myocardial fibrosis. Twit Text FOAVip MiR-33 promotes myocardial fibrosis by inhibiting MMP16 and stimulating p38 MAPK signaling ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=29774121 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29774121 #FOAvip English Wikipedia <ref>{{Cite pmid|29774121}}</ref> MiR-33 promotes myocardial fibrosis by inhibiting MMP16 and stimulating p38 MAPK signaling #MMPMID29774121 Chen Z; Ding HS; Guo X; Shen JJ; Fan D; Huang Y; Huang CX Oncotarget 2018[Apr]; 9 (31): 22047-57 PMID29774121show ga Myocardial fibrosis occurs in the late stages of many cardiovascular diseases, and appears to be stimulated by various microRNAs (miRNAs). We previously found that miR-33 may stimulate cardiac remodeling. Here, we examined the involvement of miR-33 in myocardial fibrosis. Proximal left coronary descending artery occlusion was performed in rat, and antagomiR-33a was injected. Primary cardiac fibroblasts were cultured and transfected with miR-33a mimics and inhibitors. miR-33a levels were increased in the rat after surgery, and collagen deposition and heart fibrosis were observed in vivo. Inhibition of miR-33a suppressed fibroblast proliferation, reduced the mRNA and protein levels of collagen-related markers in vitro and in vivo, and rescued the histological damage in vivo. A dual-luciferase reporter system showed that matrix metalloproteinase 16 (MMP16) gene was the direct target of MiR-33a. These results suggest that miR-33 promoted myocardial fibrosis by inhibiting MMP16 and stimulating p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway. MiR-33 may act as a novel therapeutic target for treating myocardial fibrosis. äMiR-33 promotes myocardial fibrosis by inhibiting MMP16 and stimulatin(epmc).pdf DeepDyve Pubget Overpricing