Evidence map›Paper›PMID 35990983›Full record

ReviewFrontiers in cardiovascular medicine2022

The cross-talk of lung and heart complications in COVID-19: Endothelial cells dysfunction, thrombosis, and treatment.

Langjiao Liu, Haijiao Jing, Xiaoming Wu, Mengqi Xiang, Valerie A Novakovic, Shuye Wang, Jialan Shi

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 10 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Langjiao LiuDepartment of Hematology, First Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, China.
Haijiao JingDepartment of Hematology, First Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, China.
Xiaoming WuDepartment of Hematology, First Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, China.
Mengqi XiangDepartment of Hematology, First Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, China.
Valerie A NovakovicDepartment of Research, VA Boston Healthcare System, Harvard Medical School, Boston, MA, United States.
Shuye WangDepartment of Hematology, First Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, China.
Jialan ShiDepartment of Hematology, First Affiliated Hospital of Harbin Medical University, Harbin Medical University, Harbin, China.
First Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CNVA Boston Healthcare System · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pandemic respiratory illness SARS-CoV-2 has increasingly been shown to be a systemic disease that can also have profound impacts on the cardiovascular system. Although associated cardiopulmonary sequelae can persist after infection, the link between viral infection and these complications remains unclear. There is now a recognized link between endothelial cell dysfunction and thrombosis. Its role in stimulating platelet activation and thrombotic inflammation has been widely reported. However, the procoagulant role of microparticles (MPs) in COVID-19 seems to have been neglected. As membrane vesicles released after cell injury or apoptosis, MPs exert procoagulant activity mainly by exposing phosphatidylserine (PS) on their lipid membranes. It can provide a catalytic surface for the assembly of the prothrombinase complex. Therefore, inhibiting PS externalization is a potential therapeutic strategy. In this paper, we describe the pathophysiological mechanism by which SARS-CoV-2 induces lung and heart complications through injury of endothelial cells, emphasizing the procoagulant effect of MPs and PS, and demonstrate the importance of early antithrombotic therapy. In addition, we will detail the mechanisms underlying hypoxia, another serious pulmonary complication related to SARS-CoV-2-induced endothelial cells injury and discuss the use of oxygen therapy. In the case of SARS-CoV-2 infection, virus invades endothelial cells through direct infection, hypoxia, imbalance of the RAAS, and cytokine storm. These factors cause endothelial cells to release MPs, form MPs storm, and eventually lead to thrombosis. This, in turn, accelerates hypoxia and cytokine storms, forming a positive feedback loop. Given the important role of thrombosis in the disease, early antithrombotic therapy is an important tool for COVID-19. It may maintain normal blood circulation, accelerating the clearance of viruses, waning the formation of MPs storm, and avoiding disease progression.

Indexed as

antithromboticcardiopulmonaryCOVID-19endothelial cellsmicroparticlesphosphatidylserinesequelae

Identifiers

PMID35990983
PMCPMC9390946
OpenAlexW4289939475

What Socratic holds

Textmetadata
LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.