Evidence map›Paper›PMID 34384544›Full record

ArticleCell2021

Erythroid mitochondrial retention triggers myeloid-dependent type I interferon in human SLE.

Simone Caielli, Jacob Cardenas, Adriana Almeida de Jesus, Jeanine Baisch, Lynnette Walters, Jean Philippe Blanck, Preetha Balasubramanian, Cristy Stagnar, Marina Ohouo, Seunghee Hong and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
11.5field-weighted citation impact, top 1% 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

125 citing papers in PubMed, 204 citations in OpenAlex.

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  16. Extracellular heme:DNA complexes promote oxidative stress and inflammation during lupus-associated hemolysis.Proceedings of the National Academy of Sciences of the United States of America · 2026
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65 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 5 institutions in 1 country.

Simone CaielliDrukier Institute for Children's Health, Weill Cornell Medicine, New York, NY, USA; Department of Pediatrics, Weill Cornell Medicine, New York, NY, USA. Electronic address: sic2011@med.cornell.edu.
Jacob CardenasBaylor Research Institute, Dallas, TX, USA.
Adriana Almeida de JesusTranslational Autoinflammatory Diseases Section, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA.
Jeanine BaischDrukier Institute for Children's Health, Weill Cornell Medicine, New York, NY, USA; Department of Pediatrics, Weill Cornell Medicine, New York, NY, USA.
Lynnette WaltersTexas Scottish Rite Hospital for Children, Dallas, TX, USA.
Jean Philippe BlanckBaylor Research Institute, Dallas, TX, USA.
Preetha BalasubramanianDrukier Institute for Children's Health, Weill Cornell Medicine, New York, NY, USA; Department of Pediatrics, Weill Cornell Medicine, New York, NY, USA.
Cristy StagnarDrukier Institute for Children's Health, Weill Cornell Medicine, New York, NY, USA; Department of Pediatrics, Weill Cornell Medicine, New York, NY, USA.
Marina OhouoDrukier Institute for Children's Health, Weill Cornell Medicine, New York, NY, USA; Department of Pediatrics, Weill Cornell Medicine, New York, NY, USA.
Seunghee HongDrukier Institute for Children's Health, Weill Cornell Medicine, New York, NY, USA; Department of Pediatrics, Weill Cornell Medicine, New York, NY, USA.
Lorien NassiTexas Scottish Rite Hospital for Children, Dallas, TX, USA; Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Katie StewartTexas Scottish Rite Hospital for Children, Dallas, TX, USA; Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Julie FullerTexas Scottish Rite Hospital for Children, Dallas, TX, USA; Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Jinghua GuDrukier Institute for Children's Health, Weill Cornell Medicine, New York, NY, USA; Department of Pediatrics, Weill Cornell Medicine, New York, NY, USA.
Jacques F BanchereauThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.
Tracey WrightTexas Scottish Rite Hospital for Children, Dallas, TX, USA; Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Raphaela Goldbach-ManskyTranslational Autoinflammatory Diseases Section, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA.
Virginia PascualDrukier Institute for Children's Health, Weill Cornell Medicine, New York, NY, USA; Department of Pediatrics, Weill Cornell Medicine, New York, NY, USA. Electronic address: vip2021@med.cornell.edu.
Cornell University · USTexas Scottish Rite Hospital for Children · USBaylor University · USNational Institutes of Health · USJackson Laboratory · US

Funding

Project 2: The Isoform repertoire and epigenome of Pediatric SLEP50AR070594 · NIAMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI Maria Virginia Pascual · 2016 to 2026
$18.6M
Principal ProjectU19AI144301 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI Maria Virginia Pascual · 2019 to 2026
$9.9M
Scientific CoreU19AI082715 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI PASCUAL, MARIA VIRGINIA · 2009 to 2018
$6.4M
NIAID NIH HHS U19 AI082715NIAID NIH HHS U19 AI144301NIAMS NIH HHS P50 AR070594
6 · The paper itself

Abstract

Emerging evidence supports that mitochondrial dysfunction contributes to systemic lupus erythematosus (SLE) pathogenesis. Here we show that programmed mitochondrial removal, a hallmark of mammalian erythropoiesis, is defective in SLE. Specifically, we demonstrate that during human erythroid cell maturation, a hypoxia-inducible factor (HIF)-mediated metabolic switch is responsible for the activation of the ubiquitin-proteasome system (UPS), which precedes and is necessary for the autophagic removal of mitochondria. A defect in this pathway leads to accumulation of red blood cells (RBCs) carrying mitochondria (Mito

Indexed as

AdolescentBasic Helix-Loop-Helix ProteinsChildChild, PreschoolEndothelial PAS Domain-Containing Protein 1ErythroblastsErythrocytesErythropoiesisHumansInterferon Type ILupus Erythematosus, SystemicMitochondriaMitophagyMyeloid CellsProteasome Endopeptidase ComplexUbiquitinBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1Interferon Type IProteasome Endopeptidase ComplexUbiquitinautoimmunityCANDLE syndromecGASHIF2ahuman erythropoiesisinterferonmitochondrial DNAmitophagyproteasomesystemic lupus erythematosus

Identifiers

PMID34384544
PMCPMC8380737
OpenAlexW3189265697

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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 OpenQuestion graph.