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MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

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    Clomipramine suppresses ACE2 HGNC-mediated SARS-CoV-2 entry MESHD

    Authors: Yuri Kato; Shigeru Yamada; Kazuhiro Nishiyama; Ayano Satsuka; Suyong Re; Daiki Tomokiyo; Jae Man Lee; Tomohiro Tanaka; Akiyuki Nishimura; Kenzo Yonemitsu; Hiroshi Asakura; Yuko Ibuki; Yumiko Imai; Noriho Kamiya; Kenji Mizuguchi; Takahiro Kusakabe; Yasunari Kanda; Motohiro Nishida

    doi:10.1101/2021.03.13.435221 Date: 2021-03-14 Source: bioRxiv

    Myocardial damage caused by the newly emerged coronavirus ( SARS-CoV-2) infection MESHD is one of key determinants of COVID-19 MESHD severity and mortality. SARS-CoV-2 entry to host cells are initiated by binding with its receptor, angiotensin converting enzyme (ACE) 2 HGNC, and the ACE2 HGNC abundance is thought to reflect the susceptibility to infection. Here, we found that clomipramine, a tricyclic antidepressant, potently inhibits SARS-CoV-2 infection MESHD and metabolic disorder MESHD in human iPS-derived cardiomyocytes. Among 13 approved drugs that we have previously identified as potential inhibitor of doxorubicin-induced cardiotoxicity MESHD, clomipramine showed the best potency to inhibit SARS-CoV-2 spike PROTEIN glycoprotein pseudovirus-stimulated ACE2 HGNC internalization. Indeed, SARS-CoV-2 infection MESHD to human iPS-derived cardiomyocytes (iPS-CMs) and TMPRSS2 HGNC-expressing VeroE6 cells were dramatically suppressed even after treatment with clomipramine. Furthermore, the combined use of clomipramine and remdesivir was revealed to synergistically suppress SARS-CoV-2 infection MESHD. Our results will provide the potentiality of clomipramine for the breakthrough treatment of severe COVID-19 MESHD.

    SARS-CoV-2 Infects Human Engineered Heart Tissues and Models COVID-19 MESHD Myocarditis

    Authors: Adam L Bailey; Oleksandr Dmytrenko; Lina Greenberg; Andrea L Bredemeyer; Pan Ma; Jing Liu; Vinay Penna; Lulu Lai; Emma S Winkler; Sanja Sviben; Erin Brooks; Ajith P Nair; Kent A Heck; Aniket S Rali; Leo Simpson; Mehrdad Saririan; Dan Hobohm; W. Tom Stump; James A Fitzpatrick; Xuping Xie; Pei-Yong Shi; J Travis Hinson; Weng-Tein Gi; Constanze Schmidt; Florian Leuschner; Chieh-Yu Lin; Michael S Diamond; Michael J Greenberg; Kory J Lavine; Pamela J. Bjorkman; Saurabh Mehandru; Paul D. Bieniasz; Marina Caskey; Michel C. Nussenzweig

    doi:10.1101/2020.11.04.364315 Date: 2020-11-05 Source: bioRxiv

    Epidemiological studies of the COVID-19 MESHD COVID-19 MESHD pandemic have revealed evidence of cardiac involvement MESHD and documented that myocardial injury MESHD and myocarditis MESHD are predictors of poor outcomes. Nonetheless, little is understood regarding SARS-CoV-2 tropism within the heart and whether cardiac complications result directly from myocardial infection MESHD. Here, we develop a human engineered heart tissue model and demonstrate that SARS-CoV-2 selectively infects cardiomyocytes. Viral infection MESHD is dependent on expression of angiotensin-I converting enzyme 2 HGNC ( ACE2 HGNC) and endosomal cysteine proteases, suggesting an endosomal mechanism of cell entry. After infection with SARS-CoV-2, engineered tissues display typical features of myocarditis MESHD, including cardiomyocyte cell death, impaired cardiac contractility MESHD, and innate immune cell activation. Consistent with these findings, autopsy tissue obtained from individuals with COVID-19 MESHD myocarditis MESHD demonstrated cardiomyocyte infection MESHD, cell death, and macrophage-predominate immune cell infiltrate. These findings establish human cardiomyocyte tropism for SARS-CoV-2 and provide an experimental platform for interrogating and mitigating cardiac complications of COVID-19 MESHD.

    The Contribution of Endothelial Dysfunction in Systemic Injury Subsequent to SARS-Cov-2 Infection MESHD

    Authors: Jessica Maiuolo; Rocco Mollace; Micaela Gliozzi; Vincenzo Musolino; Cristina Carresi; Sara Paone; Miriam Scicchitano; Roberta Macrì; Saverio Nucera; Francesca Bosco; Federica Scarano; Maria Caterina Zito; Stefano Ruga; Annamaria Tavernese; Vincenzo Mollace

    id:10.20944/preprints202010.0585.v1 Date: 2020-10-28 Source: Preprints.org

    Abstract: SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) infection MESHD is associated, alongside with lung infection MESHD and respiratory disease MESHD, to cardiovascular dysfunction MESHD that occurs at any stage of the disease. This includes ischemic MESHD heart disease MESHD, arrhythmias MESHD, and cardiomyopathies MESHD. The common pathophysiological link between SARS-CoV-2 infection MESHD and the cardiovascular events is represented by coagulation abnormalities MESHD and disruption of factors released by endothelial cells which contribute in maintaining the blood vessels into an anti-thrombotic state. Thus, early alteration of the functionality of endothelial cells, which may be found soon after SARS-CoV-2 infection MESHD, seems to represent the major target of SARS CoV-2 disease MESHD state and accounts for the systemic vascular dysfunction MESHD that leads to detrimental effect in terms of hospitalization and death accompanying the disease MESHD. In particular, the molecular interaction of SARS-CoV-2 with ACE2 HGNC receptor located in endothelial cell surface, either at the pulmonary and systemic level, leads to early impairment of endothelial function which, in turn, is followed by vascular inflammation MESHD and thrombosis MESHD of peripheral blood vessels. This highlights systemic hypoxia MESHD and further aggravates the vicious circle that compromises the development of the disease leading to irreversible tissue damage and death of patients with SARS CoV-2 infection MESHD. The review aims to assess some recent advances to define the crucial role of endothelial dysfunction in the pathogenesis of vascular complications accompanying SARS-CoV-2 infection MESHD. In particular, the molecular mechanisms associated to the interaction of SARS CoV-2 with ACE2 HGNC receptor located on the endothelial cells are highlighted to support its role in compromising endothelial cell functionality. Finally, the consequences of endothelial dysfunction in enhancing pro-inflammatory and pro-thrombotic effects of SARS-CoV-2 infection MESHD are assessed in order to identify early therapeutic interventions able to reduce the impact of the disease in high-risk patients.

    Mining transcriptomics and clinical data reveals ACE2 HGNC expression modulators and identifies cardiomyopathy as a risk factor for mortality in COVID-19 MESHD patients

    Authors: Navchetan Kaur; Boris Oskotsky; Atul J Butte; Zicheng Hu

    doi:10.1101/2020.10.20.20216150 Date: 2020-10-23 Source: medRxiv

    Angiotensin-converting enzyme 2 HGNC ( ACE2 HGNC) is the cell-entry receptor for SARS-CoV-2. It plays critical roles in both the transmission and the pathogenesis of the coronavirus disease 2019 MESHD ( COVID-19 MESHD). Comprehensive profiling of ACE2 HGNC expression patterns will help researchers to reveal risk factors of severe COVID-19 MESHD illness. While the expression of ACE2 HGNC in healthy human tissues has been well characterized, it is not known which diseases and drugs might modulate the ACE2 HGNC expression. In this study, we developed GENEVA (GENe Expression Variance Analysis), a semi-automated framework for exploring massive amounts of RNA-seq datasets. We applied GENEVA to 28,6650 publicly available RNA-seq samples to identify any previously studied experimental conditions that could directly or indirectly modulate ACE2 HGNC expression. We identified multiple drugs, genetic perturbations, and diseases that modulate the expression of ACE2 HGNC, including cardiomyopathy MESHD, HNF1A HGNC overexpression, and drug treatments with RAD140 and Itraconazole. Our unbiased meta-analysis of seven datasets confirms ACE2 HGNC up-regulation in all cardiomyopathy MESHD categories. Using electronic health records data from 3936 COVID19 MESHD patients, we demonstrate that patients with pre-existing cardiomyopathy MESHD have an increased mortality risk than age-matched patients with other cardiovascular conditions. GENEVA is applicable to any genes of interest and is freely accessible at http://www.genevatool.org .

    The Spectrum of Cardiovascular Complications in COVID-19 MESHD- A Comprehensive Literature Review

    Authors: Raja Shakeel Mushtaque; Rabia Mushtaque; Shahbano Baloch; Aadil Raza; Haseeb Bhatti; Zohaib Khan

    id:10.20944/preprints202008.0257.v1 Date: 2020-08-11 Source: Preprints.org

    A newly identified novel coronavirus named as severe acute respiratory syndrome MESHD-related coronavirus2 (SARS‐CoV 2) has given rise to the global pandemic. SARS-CoV2 which causes coronavirus disease 2019 MESHD ( COVID-19 MESHD), is a positive-stranded RNA virus with nucleocapsid. It binds to host angiotensin-converting enzyme2 HGNC (ACE2) receptor through surface glycoprotein (S PROTEIN protein). These ACE 2 HGNC receptors are attached to the cell membranes of many organs. Thus, COVID-19 MESHD does not only result in acute respiratory distress syndrome MESHD but also affects multiple organ systems, requiring a multidisciplinary approach to manage this disease. COVID-19 MESHD can damage the myocardial cells and result in fulminant myocarditis MESHD, acute cardiac injury MESHD, cardiomyopathy MESHD, heart failure MESHD, cardiogenic shock MESHD, or arrhythmia MESHD. COVID-19 MESHD seeds harmful immune response through cytokine storm leading to indirect organ damage. In this literature review, the available data is comprehended regarding cardiovascular complications in COVID-19 MESHD, and the correlation of biomarkers with the disease activity is discussed. This literature review also highlights the important treatment options and outcomes of the individual study.

The ZB MED preprint Viewer preVIEW includes all COVID-19 related preprints from medRxiv and bioRxiv, from ChemRxiv, from ResearchSquare, from arXiv and from Preprints.org and is updated on a daily basis (7am CET/CEST).
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MeSH Disease
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SARS-CoV-2 Proteins


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