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10.1540/jsmr.52.78 http://scihub22266oqcxt.onion/10.1540/jsmr.52.78 C5321852!5321852 !27818466     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27818466 &cmd=llinks): Failed to open stream: HTTP request failed! 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Significant contribution of TRPC6 channel-mediated Ca(2+) influx to the pathogenesis of Crohn s disease fibrotic stenosis |pdf=|usr=}}{{27818466 }} gab.com Text Significant contribution of TRPC6 channel-mediated Ca(2+) influx to the pathogenesis of Crohn s disease fibrotic stenosis JO: J Smooth Muscle Res http://www.kidney.de/pget.php?&tw=1&pmid=27818466 #FOAvip Intestinal fibrosis is an intractable complication of Crohn's disease (CD), and, when occurring excessively, causes severe intestinal obstruction that often necessitates surgical resection. The fibrosis is characterized by an imbalance in the turnover of extracellular matrix (ECM) components, where intestinal fibroblasts/myofibroblasts play active roles in ECM production, fibrogenesis and tissue remodeling, which eventually leads to the formation of stenotic lesions. There is however a great paucity of knowledge about how intestinal fibrosis initiates and progresses, which hampers the development of effective pharmacotherapies against CD. Recently, we explored the potential implications of transient receptor potential (TRP) channels in the pathogenesis of intestinal fibrosis, since they are known to act as cellular stress sensors/transducers affecting intracellular Ca(2+) homeostasis/dynamics, and are involved in a broad spectrum of cell pathophysiology including inflammation and tissue remodeling. In this review, we will place a particular emphasis on the intestinal fibroblast/myofibroblast TRPC6 channel to discuss its modulatory effects on fibrotic responses and therapeutic potential for anti-fibrotic treatment against CD-related stenosis. Twit Text FOAVip Significant contribution of TRPC6 channel-mediated Ca(2+) influx to the pathogenesis of Crohn s disease fibrotic stenosis ????J Smooth Muscle Res http://www.kidney.de/pget.php?&tw=1&pmid=27818466 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27818466 #FOAvip English Wikipedia <ref>{{Cite pmid|27818466 }}</ref> Significant contribution of TRPC6 channel-mediated Ca(2+) influx to the pathogenesis of Crohn s disease fibrotic stenosis #MMPMID27818466 Kurahara LH ; Hiraishi K ; Sumiyoshi M ; Doi M ; Hu Y ; Aoyagi K ; Jian Y ; Inoue R J Smooth Muscle Res 2016[]; 52 (0 ): 78-92 PMID27818466 show ga Intestinal fibrosis is an intractable complication of Crohn's disease (CD), and, when occurring excessively, causes severe intestinal obstruction that often necessitates surgical resection. The fibrosis is characterized by an imbalance in the turnover of extracellular matrix (ECM) components, where intestinal fibroblasts/myofibroblasts play active roles in ECM production, fibrogenesis and tissue remodeling, which eventually leads to the formation of stenotic lesions. There is however a great paucity of knowledge about how intestinal fibrosis initiates and progresses, which hampers the development of effective pharmacotherapies against CD. Recently, we explored the potential implications of transient receptor potential (TRP) channels in the pathogenesis of intestinal fibrosis, since they are known to act as cellular stress sensors/transducers affecting intracellular Ca(2+) homeostasis/dynamics, and are involved in a broad spectrum of cell pathophysiology including inflammation and tissue remodeling. In this review, we will place a particular emphasis on the intestinal fibroblast/myofibroblast TRPC6 channel to discuss its modulatory effects on fibrotic responses and therapeutic potential for anti-fibrotic treatment against CD-related stenosis. |Calcium/*metabolism [MESH] |Crohn Disease/drug therapy/*etiology/pathology [MESH] |Extracellular Matrix/metabolism [MESH] |Fibroblasts/physiology [MESH] |Fibrosis [MESH] |Humans [MESH] |Intestinal Obstruction/*etiology [MESH] |Intestines/cytology/*pathology [MESH] |Molecular Targeted Therapy [MESH] |Myofibroblasts/physiology [MESH] |Signal Transduction/physiology [MESH] |TRPC Cation Channels/*physiology [MESH] |TRPC6 Cation Channel [MESH]Significant contribution of TRPC6 channel-mediated Ca(2+) influx to th(epmc).pdf DeepDyve Pubget Overpricing