Evidence map›Paper›PMID 34264338›Full record

ReviewCardiovascular research2022

HDAC1: an environmental sensor regulating endothelial function.

Luke S Dunaway, Jennifer S Pollock

Open access · greenAbstract readReview
In one paragraph

Review in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

2 authors at 1 institution in 1 country.

Luke S DunawaySection of Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Kaul Genetics Building Room 802A, 720 20th Street South, Birmingham, AL 35233, USA.ORCID 0000-0002-7458-9669
Jennifer S PollockSection of Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Kaul Genetics Building Room 802A, 720 20th Street South, Birmingham, AL 35233, USA.ORCID 0000-0003-1956-0449
University of Alabama at Birmingham · US

Funding

Research Supplement to Promote DiversityP01HL136267 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POLLOCK, DAVID M · 2017 to 2021
$11.9M
PRedoctoral Interdisciplinary training in renal physiology and MEdicine (PRIME)T32DK116672 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POLLOCK, JENNIFER S · 2018 to 2022
$761k
HDAC1 Regulation of Endothelial NOF31HL149235 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DUNAWAY, LUKE STEWART · 2019 to 2021
$91k
NHLBI NIH HHS F31 HL149235NHLBI NIH HHS P01 HL136267NIDDK NIH HHS T32 DK116672
6 · The paper itself

Abstract

The histone deacetylases (HDACs) are a family of enzymes that catalyse lysine deacetylation of both histone and non-histone proteins. Here, we review, summarize, and provide perspectives on the literature regarding one such HDAC, HDAC1, in endothelial biology. In the endothelium, HDAC1 mediates the effects of external and environmental stimuli by regulating major endothelial functions such as angiogenesis, inflammatory signalling, redox homeostasis, and nitric oxide signalling. Angiogenesis is most often, but not exclusively, repressed by endothelial HDAC1. The regulation of inflammatory signalling is more complex as HDAC1 promotes or suppresses inflammatory signalling depending upon the environmental stimuli. HDAC1 is protective in models of atherosclerosis where loss of HDAC1 results in increased cytokine and cell adhesion molecule (CAM) abundance. In other models, HDAC1 promotes inflammation by increasing CAMs and repressing claudin-5 expression. Consistently, from many investigations, HDAC1 decreases antioxidant enzyme expression and nitric oxide production in the endothelium. HDAC1 decreases antioxidant enzyme expression through the deacetylation of histones and transcription factors, and also regulates nitric oxide production through regulating both the expression and activity of nitric oxide synthase 3. The HDAC1-dependent regulation of endothelial function through the deacetylation of both histone and non-histone proteins ultimately impacts whole animal physiology and health.

Indexed as

Histone Deacetylase 1Nitric OxideAnimalsAntioxidantsEndotheliumHistone DeacetylasesHistonesAntioxidantsHistone Deacetylase 1Histone DeacetylasesHistonesNitric OxideEndotheliumEnvironmental sensorHDAC1Nitric oxideRedox homeostasis

Identifiers

PMID34264338
PMCPMC9239577
OpenAlexW3180257396

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.