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10.14797/mdcj-11-3-160 http://scihub22266oqcxt.onion/10.14797/mdcj-11-3-160 C4666422!4666422 !26634023     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26634023 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Methodist+Debakey+Cardiovasc+J 2015 ; 11 (3 ): 160-5 Nephropedia Template TP {{tp|p=26634023 |t=2015. AIBP: A Novel Molecule at the Interface of Cholesterol Transport, Angiogenesis, and Atherosclerosis |pdf=|usr=}}{{26634023 }} gab.com Text AIBP: A Novel Molecule at the Interface of Cholesterol Transport, Angiogenesis, and Atherosclerosis JO: Methodist Debakey Cardiovasc J http://www.kidney.de/pget.php?&tw=1&pmid=26634023 #FOAvip Cardiovascular disease, which is often driven by hypercholesterolemia and subsequent coronary atherosclerosis, is the number-one cause of morbidity and mortality in the United States. Based on long-term epidemiological studies, high-density lipoprotein cholesterol (HDL-C) levels are inversely correlated with risk for coronary artery disease (CAD). HDL-mediated reverse cholesterol transport (RCT) is responsible for cholesterol removal from the peripheral tissues and return to the liver for final elimination.1 In atherosclerosis, intraplaque angiogenesis promotes plaque growth and increases plaque vulnerability. Conceivably, the acceleration of RCT and disruption of intraplaque angiogenesis would inhibit atherosclerosis and reduce CAD. We have identified a protein called apoA-I binding protein (AIBP) that augments HDL functionality by accelerating cholesterol efflux. Furthermore, AIBP inhibits vascular endothelial growth factor receptor 2 activation in endothelial cells and limits angiogenesis.2 The following discusses the prospect of using AIBP as a novel therapeutic approach for the treatment of CAD. Twit Text FOAVip AIBP: A Novel Molecule at the Interface of Cholesterol Transport, Angiogenesis, and Atherosclerosis ????Methodist Debakey Cardiovasc J http://www.kidney.de/pget.php?&tw=1&pmid=26634023 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26634023 #FOAvip English Wikipedia <ref>{{Cite pmid|26634023 }}</ref> AIBP: A Novel Molecule at the Interface of Cholesterol Transport, Angiogenesis, and Atherosclerosis #MMPMID26634023 Zhu L ; Fang L Methodist Debakey Cardiovasc J 2015[Jul]; 11 (3 ): 160-5 PMID26634023 show ga Cardiovascular disease, which is often driven by hypercholesterolemia and subsequent coronary atherosclerosis, is the number-one cause of morbidity and mortality in the United States. Based on long-term epidemiological studies, high-density lipoprotein cholesterol (HDL-C) levels are inversely correlated with risk for coronary artery disease (CAD). HDL-mediated reverse cholesterol transport (RCT) is responsible for cholesterol removal from the peripheral tissues and return to the liver for final elimination.1 In atherosclerosis, intraplaque angiogenesis promotes plaque growth and increases plaque vulnerability. Conceivably, the acceleration of RCT and disruption of intraplaque angiogenesis would inhibit atherosclerosis and reduce CAD. We have identified a protein called apoA-I binding protein (AIBP) that augments HDL functionality by accelerating cholesterol efflux. Furthermore, AIBP inhibits vascular endothelial growth factor receptor 2 activation in endothelial cells and limits angiogenesis.2 The following discusses the prospect of using AIBP as a novel therapeutic approach for the treatment of CAD. |*Neovascularization, Pathologic [MESH] |Animals [MESH] |Arteries/drug effects/*metabolism/pathology/physiopathology [MESH] |Atherosclerosis/drug therapy/*metabolism/pathology/physiopathology [MESH] |Carrier Proteins/*metabolism/therapeutic use [MESH] |Cholesterol, HDL/*metabolism [MESH] |Humans [MESH] |Models, Animal [MESH] |Racemases and Epimerases [MESH] |Signal Transduction [MESH] |Vascular Endothelial Growth Factor Receptor-2/metabolism [MESH]AIBP: A Novel Molecule at the Interface of Cholesterol Transport, Angi(epmc).pdf DeepDyve Pubget Overpricing