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10.1073/pnas.2012854118 http://scihub22266oqcxt.onion/10.1073/pnas.2012854118 33500351!7865138!33500351     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33500351&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Proc+Natl+Acad+Sci+U+S+A 2021 ; 118 (5): ? Nephropedia Template TP {{tp|p=33500351|t=2021. GRK5 is a regulator of fibroblast activation and cardiac fibrosis |pdf=|usr=}}{{33500351}} gab.com Text GRK5 is a regulator of fibroblast activation and cardiac fibrosis JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=33500351 #FOAvip Pathological remodeling of the heart is a hallmark of chronic heart failure (HF) and these structural changes further perpetuate the disease. Cardiac fibroblasts are the critical cell type that is responsible for maintaining the structural integrity of the heart. Stress conditions, such as a myocardial infarction (MI), can activate quiescent fibroblasts into synthetic and contractile myofibroblasts. G protein-coupled receptor kinase 5 (GRK5) is an important mediator of cardiovascular homeostasis through dampening of GPCR signaling, and is expressed in the heart and up-regulated in human HF. Of note, GRK5 has been demonstrated to translocate to the nucleus in cardiomyocytes in a calcium-calmodulin (Ca(2+)-CAM)-dependent manner, promoting hypertrophic gene transcription through activation of nuclear factor of activated T cells (NFAT). Interestingly, NFAT is also involved in fibroblast activation. GRK5 is highly expressed and active in cardiac fibroblasts; however, its pathophysiological role in these crucial cardiac cells is unknown. We demonstrate using adult cardiac fibroblasts that genetic deletion of GRK5 inhibits angiotensin II (AngII)-mediated fibroblast activation. Fibroblast-specific deletion of GRK5 in mice led to decreased fibrosis and cardiac hypertrophy after chronic AngII infusion or after ischemic injury compared to nontransgenic littermate controls (NLCs). Mechanistically, we show that nuclear translocation of GRK5 is involved in fibroblast activation. These data demonstrate that GRK5 is a regulator of fibroblast activation in vitro and cardiac fibrosis in vivo. This adds to previously published data which demonstrate the potential beneficial effects of GRK5 inhibition in the context of cardiac disease. Twit Text FOAVip GRK5 is a regulator of fibroblast activation and cardiac fibrosis ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=33500351 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33500351 #FOAvip English Wikipedia <ref>{{Cite pmid|33500351}}</ref> GRK5 is a regulator of fibroblast activation and cardiac fibrosis #MMPMID33500351 Eguchi A; Coleman R; Gresham K; Gao E; Ibetti J; Chuprun JK; Koch WJ Proc Natl Acad Sci U S A 2021[Feb]; 118 (5): ? PMID33500351show ga Pathological remodeling of the heart is a hallmark of chronic heart failure (HF) and these structural changes further perpetuate the disease. Cardiac fibroblasts are the critical cell type that is responsible for maintaining the structural integrity of the heart. Stress conditions, such as a myocardial infarction (MI), can activate quiescent fibroblasts into synthetic and contractile myofibroblasts. G protein-coupled receptor kinase 5 (GRK5) is an important mediator of cardiovascular homeostasis through dampening of GPCR signaling, and is expressed in the heart and up-regulated in human HF. Of note, GRK5 has been demonstrated to translocate to the nucleus in cardiomyocytes in a calcium-calmodulin (Ca(2+)-CAM)-dependent manner, promoting hypertrophic gene transcription through activation of nuclear factor of activated T cells (NFAT). Interestingly, NFAT is also involved in fibroblast activation. GRK5 is highly expressed and active in cardiac fibroblasts; however, its pathophysiological role in these crucial cardiac cells is unknown. We demonstrate using adult cardiac fibroblasts that genetic deletion of GRK5 inhibits angiotensin II (AngII)-mediated fibroblast activation. Fibroblast-specific deletion of GRK5 in mice led to decreased fibrosis and cardiac hypertrophy after chronic AngII infusion or after ischemic injury compared to nontransgenic littermate controls (NLCs). Mechanistically, we show that nuclear translocation of GRK5 is involved in fibroblast activation. These data demonstrate that GRK5 is a regulator of fibroblast activation in vitro and cardiac fibrosis in vivo. This adds to previously published data which demonstrate the potential beneficial effects of GRK5 inhibition in the context of cardiac disease. |Angiotensin II[MESH] |Animals[MESH] |Animals, Newborn[MESH] |Cardiomegaly/complications/pathology/physiopathology[MESH] |Cell Transdifferentiation[MESH] |Fibroblasts/*metabolism/*pathology[MESH] |Fibrosis[MESH] |G-Protein-Coupled Receptor Kinase 5/*metabolism[MESH] |Mice[MESH] |Mice, Knockout[MESH] |Models, Biological[MESH] |Myocardial Ischemia/complications/pathology/physiopathology[MESH] |Myocardium/*pathology[MESH] |Myofibroblasts/pathology[MESH]GRK5 is a regulator of fibroblast activation and cardiac fibrosis (epmc).pdf DeepDyve Pubget Overpricing