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10.1007/978-3-319-63245-2_18 http://scihub22266oqcxt.onion/10.1007/978-3-319-63245-2_18 29047094!7398047!29047094     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29047094&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 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 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Adv+Exp+Med+Biol 2017 ; 967 (ä): 299-314 Nephropedia Template TP {{tp|p=29047094|t=2017. Endothelial Cell Reactive Oxygen Species and Ca(2+) Signaling in Pulmonary Hypertension |pdf=|usr=}}{{29047094}} gab.com Text Endothelial Cell Reactive Oxygen Species and Ca(2+) Signaling in Pulmonary Hypertension JO: Adv Exp Med Biol http://www.kidney.de/pget.php?&tw=1&pmid=29047094 #FOAvip Pulmonary hypertension (PH) refers to a disorder characterized by elevated pulmonary arterial pressure, leading to right ventricular overload and eventually right ventricular failure, which results in high morbidity and mortality. PH is associated with heterogeneous etiologies and distinct molecular mechanisms, including abnormal migration and proliferation of endothelial and smooth muscle cells. Although the exact details are not fully elucidated, reactive oxygen species (ROS) have been shown to play a key role in promoting abnormal function in pulmonary arterial smooth muscle and endothelial cells in PH. In endothelial cells, ROS can be generated from sources such as NADPH oxidase and mitochondria, which in turn can serve as signaling molecules in a wide variety of processes including posttranslational modification of proteins involved in Ca(2+) homeostasis. In this chapter, we discuss the role of ROS in promoting abnormal vasoreactivity and endothelial migration and proliferation in various models of PH. Furthermore, we draw particular attention to the role of ROS-induced increases in intracellular Ca(2+) concentration in the pathobiology of PH. Twit Text FOAVip Endothelial Cell Reactive Oxygen Species and Ca(2+) Signaling in Pulmonary Hypertension ????Adv Exp Med Biol http://www.kidney.de/pget.php?&tw=1&pmid=29047094 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29047094 #FOAvip English Wikipedia <ref>{{Cite pmid|29047094}}</ref> Endothelial Cell Reactive Oxygen Species and Ca(2+) Signaling in Pulmonary Hypertension #MMPMID29047094 Suresh K; Shimoda LA Adv Exp Med Biol 2017[]; 967 (ä): 299-314 PMID29047094show ga Pulmonary hypertension (PH) refers to a disorder characterized by elevated pulmonary arterial pressure, leading to right ventricular overload and eventually right ventricular failure, which results in high morbidity and mortality. PH is associated with heterogeneous etiologies and distinct molecular mechanisms, including abnormal migration and proliferation of endothelial and smooth muscle cells. Although the exact details are not fully elucidated, reactive oxygen species (ROS) have been shown to play a key role in promoting abnormal function in pulmonary arterial smooth muscle and endothelial cells in PH. In endothelial cells, ROS can be generated from sources such as NADPH oxidase and mitochondria, which in turn can serve as signaling molecules in a wide variety of processes including posttranslational modification of proteins involved in Ca(2+) homeostasis. In this chapter, we discuss the role of ROS in promoting abnormal vasoreactivity and endothelial migration and proliferation in various models of PH. Furthermore, we draw particular attention to the role of ROS-induced increases in intracellular Ca(2+) concentration in the pathobiology of PH. |*Signal Transduction[MESH] |Animals[MESH] |Calcium/*metabolism[MESH] |Cell Proliferation[MESH] |Endothelial Cells/*metabolism[MESH] |Humans[MESH] |Hypertension, Pulmonary/*metabolism/physiopathology[MESH] |Mitochondria/metabolism[MESH] |Oxidation-Reduction[MESH]Endothelial Cell Reactive Oxygen Species and Ca(2+) Signaling in Pulmo(epmc).pdf DeepDyve Pubget Overpricing