<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Gkogkou, Eirini</style></author><author><style face="normal" font="default" size="100%">Barnasas, Grigoris</style></author><author><style face="normal" font="default" size="100%">Vougas, Konstantinos</style></author><author><style face="normal" font="default" size="100%">Trougakos, Ioannis P.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">{Expression profiling meta-analysis of ACE2 and TMPRSS2, the putative anti-inflammatory receptor and priming protease of SARS-CoV-2 in human cells, and identification of putative modulators}</style></title><secondary-title><style face="normal" font="default" size="100%">Redox Biology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">ACE2</style></keyword><keyword><style  face="normal" font="default" size="100%">Covid-19</style></keyword><keyword><style  face="normal" font="default" size="100%">CTSB/L</style></keyword><keyword><style  face="normal" font="default" size="100%">gene expression</style></keyword><keyword><style  face="normal" font="default" size="100%">SARS-CoV-2</style></keyword><keyword><style  face="normal" font="default" size="100%">TMPRSS2</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2020</style></year><pub-dates><date><style  face="normal" font="default" size="100%">sep</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">https://doi.org/10.1016/j.redox.2020.101615 https://linkinghub.elsevier.com/retrieve/pii/S221323172030820X</style></url></web-urls></urls><publisher><style face="normal" font="default" size="100%">Elsevier B.V.</style></publisher><volume><style face="normal" font="default" size="100%">36</style></volume><pages><style face="normal" font="default" size="100%">101615</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has resulted in hundreds of thousands of deaths worldwide. While the majority of people with COVID-19 won't require hospitalization, those who do may experience severe life-threatening complications, including acute respiratory distress syndrome. SARS-CoV-2 infects human cells by binding to the cellular surface protein angiotensin-converting enzyme 2 (ACE2); in addition, the cellular transmembrane serine protease 2 (TMPRSS2) is needed for priming of the spike (S) protein of the virus. Virus entry may also depend on the activity of the endosomal/lysosomal cysteine proteases cathepsin B, L (CTSB, CTSL) although their activity is likely dispensable. Given that the uncertainty of how COVID-19 kills, hampers doctors' ability to choose treatments the need for a deep understanding of COVID-19 biology is urgent. Herein, we performed an expression profiling meta-analysis of ACE2, TMPRSS2 and CTSB/L genes (and proteins) in public repository databases and found that all are widely expressed in human tissues; also, the ACE2 and TMPRSS2 genes tend to be co-regulated. The ACE2 and TMPRSS genes expression is (among others) suppressed by TNF, and is induced by pro-inflammatory conditions including obesity, Barrett's esophagus, stomach infection by helicobacter pylori, diabetes, autoimmune diseases and oxidized LDL; by exercise, as well as by growth factors, viruses' infections, cigarette smoke, interferons and androgens. Regarding currently investigated therapies interferon-beta induced ACE2 gene expression in bronchial epithelial cells, while chloroquine tends to upregulate CTSB/L genes. Finally, we analyzed KEGG pathways modulated by ACE2, TMPRSS2 and CTSB/L and probed DrugBank for drugs that target modules of the affected pathways. Our data indicate possible novel high-risk groups for COVID-19; provide a rich resource for future investigations of its pathogenesis and highlight the therapeutic challenges we face.</style></abstract></record></records></xml>