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10.1007/s11897-017-0329-9 http://scihub22266oqcxt.onion/10.1007/s11897-017-0329-9 C5423965!5423965!28447290     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Curr+Heart+Fail+Rep 2017 ; 14 (3): 167-78 Nephropedia Template TP {{tp|p=28447290|t=2017. Regulation of Cardiomyocyte T-Tubular Structure: Opportunities for Therapy |pdf=|usr=}}{{28447290}} gab.com Text Regulation of Cardiomyocyte T-Tubular Structure: Opportunities for Therapy JO: Curr Heart Fail Rep http://www.kidney.de/pget.php?&tw=1&pmid=28447290 #FOAvip Purpose of Review: Membrane invaginations called t-tubules play an integral role in triggering cardiomyocyte contraction, and their disruption during diseases such as heart failure critically impairs cardiac performance. In this review, we outline the growing understanding of the malleability of t-tubule structure and function, and highlight emerging t-tubule regulators which may be exploited for novel therapies. Recent Findings: New technologies are revealing the nanometer scale organization of t-tubules, and their functional junctions with the sarcoplasmic reticulum called dyads, which generate Ca2+ sparks. Recent data have indicated that the dyadic anchoring protein junctophilin-2, and the membrane-bending protein BIN1 are key regulators of dyadic formation and maintenance. While the underlying signals which control expression and localization of these proteins remain unclear, accumulating data support an important role of myocardial workload. Summary: Although t-tubule alterations are believed to be a key cause of heart failure, the plasticity of these structures also creates an opportunity for therapy. Promising recent data suggest that such therapies may specifically target junctophilin-2, BIN1, and/or mechanotransduction. Twit Text FOAVip Regulation of Cardiomyocyte T-Tubular Structure: Opportunities for Therapy ????Curr Heart Fail Rep http://www.kidney.de/pget.php?&tw=1&pmid=28447290 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28447290 #FOAvip English Wikipedia <ref>{{Cite pmid|28447290}}</ref> Regulation of Cardiomyocyte T-Tubular Structure: Opportunities for Therapy #MMPMID28447290 Manfra O; Frisk M; Louch WE Curr Heart Fail Rep 2017[]; 14 (3): 167-78 PMID28447290show ga Purpose of Review: Membrane invaginations called t-tubules play an integral role in triggering cardiomyocyte contraction, and their disruption during diseases such as heart failure critically impairs cardiac performance. In this review, we outline the growing understanding of the malleability of t-tubule structure and function, and highlight emerging t-tubule regulators which may be exploited for novel therapies. Recent Findings: New technologies are revealing the nanometer scale organization of t-tubules, and their functional junctions with the sarcoplasmic reticulum called dyads, which generate Ca2+ sparks. Recent data have indicated that the dyadic anchoring protein junctophilin-2, and the membrane-bending protein BIN1 are key regulators of dyadic formation and maintenance. While the underlying signals which control expression and localization of these proteins remain unclear, accumulating data support an important role of myocardial workload. Summary: Although t-tubule alterations are believed to be a key cause of heart failure, the plasticity of these structures also creates an opportunity for therapy. Promising recent data suggest that such therapies may specifically target junctophilin-2, BIN1, and/or mechanotransduction. äRegulation of Cardiomyocyte T-Tubular Structure: Opportunities for The(epmc).pdf DeepDyve Pubget Overpricing