Evidence map›Paper›PMID 31235857›Full record

ArticleCell death and differentiation2020

The NuRD chromatin-remodeling complex enzyme CHD4 prevents hypoxia-induced endothelial Ripk3 transcription and murine embryonic vascular rupture.

Sarah Colijn, Siqi Gao, Kyle G Ingram, Matthew Menendez, Vijay Muthukumar, Robert Silasi-Mansat, Joanna J Chmielewska, Myron Hinsdale, Florea Lupu, Courtney T Griffin

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. RIPK3 Contributes to Thyroid Hormone-Induced Photoreceptor Degeneration.International journal of molecular sciences · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. RIPK3 signaling and its role in the pathogenesis of cancers.Cellular and molecular life sciences : CMLS · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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

10 authors at 3 institutions in 2 countries.

Sarah Colijn *Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Siqi Gao *Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Kyle G Ingram *Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Matthew MenendezCardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Vijay MuthukumarCardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Robert Silasi-MansatCardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Joanna J ChmielewskaCardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Myron HinsdaleDepartment of Physiological Sciences, Oklahoma State University, Stillwater, OK, 74078, USA.
Florea LupuCardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA.
Courtney T GriffinCardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, USA. courtney-griffin@omrf.org.ORCID http://orcid.org/0000-0001-8100-3171
Oklahoma Medical Research Foundation · USOklahoma State University · USStowers Institute for Medical Research · US

Funding

Interdisciplinary research in vascular biologyP20GM103441 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI MCEVER, RODGER PAUL · 2012 to 2014
$7.3M
Pilot ProjectP30GM114731 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI LUPU, FLOREA · 2016 to 2020
$6.5M
Protease-Mediated Vascular Instability in Development and DiseaseR35HL144605 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GRIFFIN, COURTNEY T · 2019 to 2025
$5.9M
Regulation of Venous and Lymphatic Identity by Chromatin-RemodelingR01HL111178 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GRIFFIN, COURTNEY T · 2012 to 2016
$2.1M
Epigenetic regulation of endothelial cell necroptosis impacts vascular integrityR01HL134778 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GRIFFIN, COURTNEY T · 2017 to 2018
$870k
NHLBI NIH HHS R01 HL111178NHLBI NIH HHS R01 HL134778NHLBI NIH HHS R35 HL144605NIGMS NIH HHS P20 GM103441NIGMS NIH HHS P30 GM114731
6 · The paper itself

Abstract

Physiological hypoxia can trigger transcriptional events that influence many developmental processes during mammalian embryogenesis. One way that hypoxia affects transcription is by engaging chromatin-remodeling complexes. We now report that chromodomain helicase DNA binding protein 4 (CHD4), an enzyme belonging to the nucleosome remodeling and deacetylase (NuRD) chromatin-remodeling complex, is required for transcriptional repression of the receptor-interacting protein kinase 3 (Ripk3)-a critical executor of the necroptosis cell death program-in hypoxic murine embryonic endothelial cells. Genetic deletion of Chd4 in murine embryonic endothelial cells in vivo results in upregulation of Ripk3 transcripts and protein prior to vascular rupture and lethality at midgestation, and concomitant deletion of Ripk3 partially rescues these phenotypes. In addition, CHD4 binds to and prevents acetylation of the Ripk3 promoter in cultured endothelial cells grown under hypoxic conditions to prevent excessive Ripk3 transcription. These data demonstrate that excessive RIPK3 is detrimental to embryonic vascular integrity and indicate that CHD4 suppresses Ripk3 transcription when the embryonic environment is particularly hypoxic prior to the establishment of fetal-placental circulation at midgestation. Altogether, this research provides new insights into regulators of Ripk3 transcription and encourages future studies into the mechanism by which excessive RIPK3 damages embryonic blood vessels.

Indexed as

AnimalsCell HypoxiaCells, CulturedChromatinDNA HelicasesEmbryonic Stem CellsEndothelial CellsMi-2 Nucleosome Remodeling and Deacetylase ComplexMiceMice, KnockoutMice, TransgenicReceptor-Interacting Protein Serine-Threonine KinasesChromatinDNA HelicasesMi-2beta protein, mouseMi-2 Nucleosome Remodeling and Deacetylase ComplexReceptor-Interacting Protein Serine-Threonine KinasesRipk3 protein, mouse

Identifiers

PMID31235857
PMCPMC7206092
OpenAlexW2949326027

What OpenQuestion holds

Textmetadata
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.