Evidence map›Paper›PMID 33345622›Full record

ArticleAnnals of medicine2021

Increased expression of hypoxia-induced factor 1α mRNA and its related genes in myeloid blood cells from critically ill COVID-19 patients.

Keiko Taniguchi-Ponciano, Eduardo Vadillo, Héctor Mayani, César Raúl Gonzalez-Bonilla, Javier Torres, Abraham Majluf, Guillermo Flores-Padilla, Niels Wacher-Rodarte, Juan Carlos Galan, Eduardo Ferat-Osorio and 15 more

Open access · hybridAbstract read
In one paragraph

Article in Annals of medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.3field-weighted citation impact, top 11% 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

38 citing papers in PubMed, 58 citations in OpenAlex.

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  19. Stem cell therapy for COVID-19 pneumonia.Molecular biomedicine · 2022
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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

25 authors at 4 institutions in 3 countries.

Keiko Taniguchi-PoncianoUnidad de Investigación Médica en Enfermedades Endocrinas, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Eduardo VadilloUnidad de Investigación Médica en Enfermedades Oncológicas, UMAE Hospital de Oncología, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Héctor MayaniUnidad de Investigación Médica en Enfermedades Oncológicas, UMAE Hospital de Oncología, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
César Raúl Gonzalez-BonillaTitular, Coordinación de Investigación en Salud, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Javier TorresUnidad de Investigación Médica en Enfermedades Infecciosas y Parasitarias, UMAE Hospital de Pediatría, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Abraham MajlufUnidad de Investigación Médica en trombosis, hemostasia y aterogénesis, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Guillermo Flores-PadillaServicio de Medicina Interna, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Niels Wacher-RodarteUnidad de Investigación Médica en Epidemiología Clínica, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Juan Carlos GalanServicio de Medicina Interna, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Eduardo Ferat-OsorioDivisión de Investigación en Salud, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Francisco Blanco-FavelaUnidad de Investigación Médica en Inmunología, UMAE Hospital de Pediatría, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Constantino Lopez-MaciasUnidad de Investigación Médica en Inmunoquímica, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Aldo Ferreira-HermosilloUnidad de Investigación Médica en Enfermedades Endocrinas, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Claudia Ramirez-RenteriaUnidad de Investigación Médica en Enfermedades Endocrinas, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Eduardo Peña-MartínezUnidad de Investigación Médica en Enfermedades Endocrinas, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Gloria Silva-RománUnidad de Investigación Médica en Enfermedades Endocrinas, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Sandra Vela-PatiñoUnidad de Investigación Médica en Enfermedades Endocrinas, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Carlos Mata-LozanoUnidad de Investigación Médica en Enfermedades Endocrinas, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Roberto Carvente-GarciaUnidad de Investigación Médica en Enfermedades Endocrinas, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Lourdes Basurto-AcevedoUnidad de Investigación Médica en Enfermedades Endocrinas, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Renata SaucedoUnidad de Investigación Médica en Enfermedades Endocrinas, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Patricia Piña-SanchezUnidad de Investigación Médica en Enfermedades Oncológicas, UMAE Hospital de Oncología, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Antonieta Chavez-GonzalezUnidad de Investigación Médica en Enfermedades Oncológicas, UMAE Hospital de Oncología, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Daniel Marrero-RodríguezUnidad de Investigación Médica en Enfermedades Endocrinas, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Moisés MercadoUnidad de Investigación Médica en Enfermedades Endocrinas, UMAE Hospital de Especialidades, Centro Medico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico city, Mexico.
Centro Medico Nacional Siglo XXI · MXMexican Social Security Institute · MXHospital de Especialidades · MXSociedad Española de Trombosis y Hemostasia · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCOVID-19 counts 46 million people infected and killed more than 1.2 million. Hypoxaemia is one of the main clinical manifestations, especially in severe cases. HIF1α is a master transcription factor involved in the cellular response to oxygen levels. The immunopathogenesis of this severe form of COVID-19 is poorly understood.

methodsWe performed scRNAseq from leukocytes from five critically ill COVID-19 patients and characterized the expression of hypoxia-inducible factor1α and its transcriptionally regulated genes. Also performed metanalysis from the publicly available RNAseq data from COVID-19 bronchoalveolar cells.

resultsCritically-ill COVID-19 patients show a shift towards an immature myeloid profile in peripheral blood cells, including band neutrophils, immature monocytes, metamyelocytes, monocyte-macrophages, monocytoid precursors, and promyelocytes-myelocytes, together with mature monocytes and segmented neutrophils. May be the result of a physiological response known as emergency myelopoiesis. These cellular subsets and bronchoalveolar cells express HIF1α and their transcriptional targets related to inflammation (CXCL8, CXCR1, CXCR2, and CXCR4); virus sensing, (TLR2 and TLR4); and metabolism (SLC2A3, PFKFB3, PGK1, GAPDH and SOD2).

conclusionsThe up-regulation and participation of HIF1α in events such as inflammation, immunometabolism, and TLR make it a potential molecular marker for COVID-19 severity and, interestingly, could represent a potential target for molecular therapy. Key messages Critically ill COVID-19 patients show emergency myelopoiesis. HIF1α and its transcriptionally regulated genes are expressed in immature myeloid cells which could serve as molecular targets. HIF1α and its transcriptionally regulated genes is also expressed in lung cells from critically ill COVID-19 patients which may partially explain the hypoxia related events.

Indexed as

Critical IllnessCOVID-19FemaleHumansHypoxia-Inducible Factor 1, alpha SubunitMaleMyeloid CellsReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSequence Analysis, RNAUp-RegulationHypoxia-Inducible Factor 1, alpha SubunitRNA, MessengerCOVID-19critically illHIF1αimmature myeloid cellsSARS-CoV-2scRNAseq

Identifiers

PMID33345622
PMCPMC7784832
OpenAlexW3116920768

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