Evidence map›Paper›PMID 38511328›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2024

Monocyte-Mediated Thrombosis Linked to Circulating Tissue Factor and Immune Paralysis in COVID-19.

Sascha N Goonewardena, Qinzhong Chen, Ashley M Tate, Olga G Grushko, Dilna Damodaran, Pennelope K Blakely, Salim S Hayek, David J Pinsky, Robert S Rosenson

Open access · greenAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 10 citations in OpenAlex.

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  10. COVID-19: a vascular nightmare unfolding.Frontiers in immunology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Sascha N GoonewardenaDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor (S.N.G., A.M.T., O.G.G., D.D., P.K.B., S.S.H., D.J.P.).ORCID 0000-0002-3772-8818
Qinzhong ChenMetabolism and Lipids Unit, Cardiovascular Institute, Marie-Josee and Henry R. Kravis Center for Cardiovascular Health, Icahn School of Medicine at Mount Sinai, New York, NY (Q.C., R.S.R.).ORCID 0000-0001-7814-9145
Ashley M TateDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor (S.N.G., A.M.T., O.G.G., D.D., P.K.B., S.S.H., D.J.P.).ORCID 0000-0002-0096-741X
Olga G GrushkoDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor (S.N.G., A.M.T., O.G.G., D.D., P.K.B., S.S.H., D.J.P.).ORCID 0000-0002-9330-1798
Dilna DamodaranDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor (S.N.G., A.M.T., O.G.G., D.D., P.K.B., S.S.H., D.J.P.).ORCID 0000-0002-2735-6803
Pennelope K BlakelyDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor (S.N.G., A.M.T., O.G.G., D.D., P.K.B., S.S.H., D.J.P.).ORCID 0000-0002-9677-3010
Salim S HayekDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor (S.N.G., A.M.T., O.G.G., D.D., P.K.B., S.S.H., D.J.P.).ORCID 0000-0003-0180-349X
David J PinskyDivision of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor (S.N.G., A.M.T., O.G.G., D.D., P.K.B., S.S.H., D.J.P.).
Robert S RosensonMetabolism and Lipids Unit, Cardiovascular Institute, Marie-Josee and Henry R. Kravis Center for Cardiovascular Health, Icahn School of Medicine at Mount Sinai, New York, NY (Q.C., R.S.R.).ORCID 0000-0002-5599-0633
Michigan Medicine · USCardiovascular Institute of the South · USGfK (United States) · USG. H. Gillespie Associates (United States) · US

Funding

ACTIV Integration of Host-targeting Therapies for COVID-19 Administrative Coordinating CenterOT2HL156812 · NHLBI · RESEARCH TRIANGLE INSTITUTE · PI NOLEN, TRACY L, THOMAS, SONIA M · 2020 to 2024
$1270.7M
Purinergic regulation of Innate Immunity to promote Venous HomeostasisR01HL150392 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PINSKY, DAVID J. · 2020 to 2024
$2.2M
Coordination of cardiac inflammation/remodeling in heart failure by myeloid catabolism of purinergic DAMPsI01CX002560 · VA · VETERANS HEALTH ADMINISTRATION · PI Sascha Nilu Goonewardena · 2024 to 2026
–
CSRD VA I01 CX002560NHLBI NIH HHS OT2 HL156812NHLBI NIH HHS R01 HL150392
6 · The paper itself

Abstract

backgroundSARS-CoV-2 infections cause COVID-19 and are associated with inflammation, coagulopathy, and high incidence of thrombosis. Myeloid cells help coordinate the initial immune response in COVID-19. Although we appreciate that myeloid cells lie at the nexus of inflammation and thrombosis, the mechanisms that unite the two in COVID-19 remain largely unknown.

methodsIn this study, we used systems biology approaches including proteomics, transcriptomics, and mass cytometry to define the circulating proteome and circulating immune cell phenotypes in subjects with COVID-19.

resultsIn a cohort of subjects with COVID-19 (n=35), circulating markers of inflammation (CCL23 [C-C motif chemokine ligand 23] and IL [interleukin]-6) and vascular dysfunction (ACE2 [angiotensin-converting enzyme 2] and TF [tissue factor]) were elevated in subjects with severe compared with mild COVID-19. Additionally, although the total white blood cell counts were similar between COVID-19 groups, CD14+ (cluster of differentiation) monocytes from subjects with severe COVID-19 expressed more TF. At baseline, transcriptomics demonstrated increased IL-6, CCL3, ACOD1 (aconitate decarboxylase 1), C5AR1 (complement component 5a receptor), C5AR2, and TF in subjects with severe COVID-19 compared with controls. Using stress transcriptomics, we found that circulating immune cells from subjects with severe COVID-19 had evidence of profound immune paralysis with greatly reduced transcriptional activation and release of inflammatory markers in response to TLR (Toll-like receptor) activation. Finally, sera from subjects with severe (but not mild) COVID-19 activated human monocytes and induced TF expression.

conclusionsTaken together, these observations further elucidate the pathological mechanisms that underlie immune dysfunction and coagulation abnormalities in COVID-19, contributing to our growing understanding of SARS-CoV-2 infections that could also be leveraged to develop novel diagnostic and therapeutic strategies.

Indexed as

COVID-19MonocytesThromboplastinThrombosisAdultAgedBiomarkersFemaleHumansMaleMiddle AgedProteomicsSARS-CoV-2BiomarkersThromboplastinimmunityinflammationparalysissystems biologythrombosis

Identifiers

PMID38511328
PMCPMC11043007
OpenAlexW4393055179

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.