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10.1016/j.yjmcc.2021.11.010 http://scihub22266oqcxt.onion/10.1016/j.yjmcc.2021.11.010 34838588!8610843!34838588     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34838588&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       J+Mol+Cell+Cardiol 2022 ; 164 (ä): 69-82 Nephropedia Template TP {{tp|p=34838588|t=2022. Endothelial contribution to COVID-19: an update on mechanisms and therapeutic implications |pdf=|usr=}}{{34838588}} gab.com Text Endothelial contribution to COVID-19: an update on mechanisms and therapeutic implications JO: J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=34838588 #FOAvip The global propagation of SARS-CoV-2 leads to an unprecedented public health emergency. Despite that the lungs are the primary organ targeted by COVID-19, systemic endothelial inflammation and dysfunction is observed particularly in patients with severe COVID-19, manifested by elevated endothelial injury markers, endotheliitis, and coagulopathy. Here, we review the clinical characteristics of COVID-19 associated endothelial dysfunction; and the likely pathological mechanisms underlying the disease including direct cell entry or indirect immune overreactions after SARS-CoV-2 infection. In addition, we discuss potential biomarkers that might indicate the disease severity, particularly related to the abnormal development of thrombosis that is a fatal vascular complication of severe COVID-19. Furthermore, we summarize clinical trials targeting the direct and indirect pathological pathways after SARS-CoV-2 infection to prevent or inhibit the virus induced endothelial disorders. Twit Text FOAVip Endothelial contribution to COVID-19: an update on mechanisms and therapeutic implications ????J Mol Cell Cardiol http://www.kidney.de/pget.php?&tw=1&pmid=34838588 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34838588 #FOAvip English Wikipedia <ref>{{Cite pmid|34838588}}</ref> Endothelial contribution to COVID-19: an update on mechanisms and therapeutic implications #MMPMID34838588 Ma Z; Yang KY; Huang Y; Lui KO J Mol Cell Cardiol 2022[Mar]; 164 (ä): 69-82 PMID34838588show ga The global propagation of SARS-CoV-2 leads to an unprecedented public health emergency. Despite that the lungs are the primary organ targeted by COVID-19, systemic endothelial inflammation and dysfunction is observed particularly in patients with severe COVID-19, manifested by elevated endothelial injury markers, endotheliitis, and coagulopathy. Here, we review the clinical characteristics of COVID-19 associated endothelial dysfunction; and the likely pathological mechanisms underlying the disease including direct cell entry or indirect immune overreactions after SARS-CoV-2 infection. In addition, we discuss potential biomarkers that might indicate the disease severity, particularly related to the abnormal development of thrombosis that is a fatal vascular complication of severe COVID-19. Furthermore, we summarize clinical trials targeting the direct and indirect pathological pathways after SARS-CoV-2 infection to prevent or inhibit the virus induced endothelial disorders. |*SARS-CoV-2[MESH] |Adolescent[MESH] |Adult[MESH] |Aged[MESH] |Angiotensin-Converting Enzyme 2/physiology[MESH] |Animals[MESH] |COVID-19/blood/complications/*pathology/physiopathology/therapy[MESH] |Clinical Trials as Topic[MESH] |Endothelial Cells/pathology/virology[MESH] |Endothelium, Vascular/immunology/*pathology/physiopathology[MESH] |HMGB1 Protein/physiology[MESH] |Humans[MESH] |Macaca mulatta[MESH] |Mice[MESH] |Neuropilin-1/physiology[MESH] |Oxidative Stress[MESH] |Reactive Oxygen Species[MESH] |Receptors, Virus/physiology[MESH] |Scavenger Receptors, Class B/physiology[MESH] |Severity of Illness Index[MESH] |Signal Transduction[MESH] |Systemic Inflammatory Response Syndrome/pathology/physiopathology[MESH] |Thrombophilia/etiology/physiopathology[MESH] |Vascular Endothelial Growth Factor A/physiology[MESH] |Vasculitis/etiology/immunology/physiopathology[MESH]Endothelial contribution to COVID-19: an update on mechanisms and ther(epmc).pdf DeepDyve Pubget Overpricing