Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

There are no SARS-CoV-2 protein terms in the subcorpus


SARS-CoV-2 Proteins
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    Excessive matrix metalloproteinase-1 HGNC and hyperactivation of endothelial cells occurred in COVID-19 MESHD patients and were associated with the severity of COVID-19 MESHD

    Authors: Fahim Syed; Wei Li; Ryan F Relich; Patrick M Russell; Shanxiang Zhang; Michelle K Zimmerman; Qigui Yu

    doi:10.1101/2021.01.19.21250115 Date: 2021-01-20 Source: medRxiv

    COVID-19 MESHD starts as a respiratory disease MESHD that can progress to pneumonia MESHD, severe acute respiratory syndrome MESHD (SARS), and multi-organ failure MESHD. Growing evidence suggests that COVID-19 MESHD is a systemic illness that primarily injures the vascular endothelium, yet the underlying mechanisms remain unknown. SARS-CoV-2 infection MESHD is believed to trigger a cytokine storm that plays a critical role in the pathogenesis of endothelialitis and vascular injury MESHD, eventually leading to respiratory and multi-organ failure MESHD in COVID-19 MESHD patients. We used a multiplex immunoassay to systematically profile and compare 65 inflammatory cytokines/chemokines/growth factors in plasma samples from 24 hospitalized (severe/critical) COVID-19 MESHD patients, 14 mild/moderate cases, and 13 healthy controls (HCs). Patients with severe/critical and mild/moderate COVID-19 MESHD had significantly higher plasma levels of 20 analytes than HCs. Surprisingly, only one cytokine ( MIF HGNC) was among these altered analytes, while the rest were chemokines and growth factors. In addition, only MMP-1 HGNC and VEGF-A HGNC were significantly elevated in hospitalized COVID-19 MESHD patients when compared to mild/moderate cases. Given that excessive MMP-1 HGNC plays a central role in tissue destruction in a wide variety of vascular diseases MESHD and that elevated VEGF-A HGNC, an EC activation marker, increases vascular permeability, we further studied MMP-1 HGNC enzymatic activity and other EC activation markers such as soluble forms of CD146 HGNC, ICAM-1 HGNC, and VCAM-1 HGNC. We found that plasma MMP-1 HGNC enzymatic activity and plasma levels of MMP-1 HGNC and EC activation markers were highly dysregulated in COVID-19 MESHD patients. Some dysregulations MESHD were associated with patients age or gender, but not with race. Our results demonstrate that COVID-19 MESHD patients have distinct inflammatory profiles that are distinguished from the cytokine storms in other human diseases. Excessive MMP-1 HGNC and hyperactivation of ECs occur in COVID-19 MESHD patients and are associated with the severity of COVID-19 MESHD.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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