Evidence mapPaperPMID 36766773Full record

ReviewCells2023

Diabetes and Its Cardiovascular Complications: Potential Role of the Acetyltransferase p300.

Nadia Di Pietrantonio, Pamela Di Tomo, Domitilla Mandatori, Gloria Formoso, Assunta Pandolfi

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Targeting the Epigenetic Remodeler GCN5 Prevents Vascular Oxidative Stress and Endothelial Dysfunction in Obesity: Insights in Patients with Cardiometabolic Disease.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. 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

5 authors at 1 institution in 1 country.

Nadia Di PietrantonioDepartment of Medical, Oral and Biotechnological Sciences, Center for Advanced Studies and Technology-CAST, University G. D'Annunzio of Chieti-Pescara, 66100 Chieti, Italy.ORCID 0000-0001-6604-0804
Pamela Di TomoDepartment of Medical, Oral and Biotechnological Sciences, Center for Advanced Studies and Technology-CAST, University G. D'Annunzio of Chieti-Pescara, 66100 Chieti, Italy.
Domitilla MandatoriDepartment of Medical, Oral and Biotechnological Sciences, Center for Advanced Studies and Technology-CAST, University G. D'Annunzio of Chieti-Pescara, 66100 Chieti, Italy.
Gloria FormosoDepartment of Medicine and Aging Sciences, Center for Advanced Studies and Technology-CAST, University G. D'Annunzio of Chieti-Pescara, 66100 Chieti, Italy.
Assunta PandolfiDepartment of Medical, Oral and Biotechnological Sciences, Center for Advanced Studies and Technology-CAST, University G. D'Annunzio of Chieti-Pescara, 66100 Chieti, Italy.ORCID 0000-0003-4135-7631
University of Chieti-Pescara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes has been shown to accelerate vascular senescence, which is associated with chronic inflammation and oxidative stress, both implicated in the development of endothelial dysfunction. This condition represents the initial alteration linking diabetes to related cardiovascular (CV) complications. Recently, it has been hypothesised that the acetyltransferase, p300, may contribute to establishing an early vascular senescent phenotype, playing a relevant role in diabetes-associated inflammation and oxidative stress, which drive endothelial dysfunction. Specifically, p300 can modulate vascular inflammation through epigenetic mechanisms and transcription factors acetylation. Indeed, it regulates the inflammatory pathway by interacting with nuclear factor kappa-light-chain-enhancer of activated B cells p65 subunit (NF-κB p65) or by inducing its acetylation, suggesting a crucial role of p300 as a bridge between NF-κB p65 and the transcriptional machinery. Additionally, p300-mediated epigenetic modifications could be upstream of the activation of inflammatory cytokines, and they may induce oxidative stress by affecting the production of reactive oxygen species (ROS). Because several in vitro and in vivo studies shed light on the potential use of acetyltransferase inhibitors, a better understanding of the mechanisms underlying the role of p300 in diabetic vascular dysfunction could help in finding new strategies for the clinical management of CV diseases related to diabetes.

Indexed as

Cardiovascular SystemDiabetes MellitusAcetyltransferasesE1A-Associated p300 ProteinHumansInflammationNF-kappa BAcetyltransferasesE1A-Associated p300 ProteinEP300 protein, humanNF-kappa Bcardiovascular diseasediabetesendothelial dysfunctionepigeneticsinflammationoxidative stressp300senescence

Identifiers

PMID36766773
PMCPMC9914144
OpenAlexW4318482070

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.