Evidence map›Paper›PMID 23826814›Full record

ArticleBritish journal of pharmacology2013

17-β Oestradiol prevents cardiovascular dysfunction in post-menopausal metabolic syndrome by affecting SIRT1/AMPK/H3 acetylation.

Dhaval Sharad Bendale, Pinakin Arun Karpe, Richa Chhabra, Sachin Prabhakarrao Shete, Heta Shah, Kulbhushan Tikoo

Abstract read
In one paragraph

Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.6field-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

45 citing papers in PubMed, 72 citations in OpenAlex.

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  15. Novel Role of the SIRT1 in Endocrine and Metabolic Diseases.International journal of biological sciences · 2023
    Review
  16. The Roles of Androgens in Humans: Biology, Metabolic Regulation and Health.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Review
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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

6 authors at 3 institutions in 1 country.

Dhaval Sharad BendaleLaboratory of Chromatin Biology, Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Mohali, Punjab, India.
Pinakin Arun Karpe
Richa Chhabra
Sachin Prabhakarrao Shete
Heta Shah
Kulbhushan Tikoo
National Institute of Pharmaceutical Education and Research · INNational Institute of Pharmaceutical Education and Research · INNational Institute of Pharmaceutical Education and Research · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeOestrogen therapy is known to induce cardioprotection in post-menopausal metabolic syndrome (PMS). Hence, we investigated the effect of 17-β oestradiol (E2) on functional responses to angiotensin II and cardiovascular dysfunction in a rat model of PMS. EXPERIMENTAL APPROACH: PMS was induced in ovariectomized rats by feeding a high-fat diet for 10 weeks. Isometric tension responses of aortic rings to angiotensin II were recorded using an isometric force transducer. TUNEL assay and immunoblotting was performed to assess apoptosis and protein expression respectively in PMS. KEY

resultsEndothelial dysfunction in PMS was characterized by enhanced angiotensin II-induced contractile responses and impaired endothelial dependent vasodilatation. This was associated with an increased protein expression of AT1 receptors in the aorta and heart in PMS. PMS induced cardiac apoptosis by activating Bax and PARP protein expression. These changes were associated with a down-regulation in the expression of silent information regulation 2 homologue (SIRT1)/P-AMP-activated PK (AMPK) and increased H3 acetylation in aorta and heart. E2 partially suppressed angiotensin II-induced contractions, restored the protein expression of SIRT1/P-AMPK and suppressed H3 acetylation. The role of SIRT1/AMPK was further highlighted by administration of sirtinol and compound C (ex vivo), which enhanced angiotensin II contractile responses and ablated the protective effect of E2 on PMS. CONCLUSION AND IMPLICATIONS: Our results provide novel mechanisms for PMS-induced cardiovascular dysfunction involving SIRT1/AMPK/ histone H3 acetylation, which was prevented by E2. The study suggests that therapies targeting SIRT1/AMPK/epigenetic modifications may be beneficial in reducing the risk of cardiovascular disorders.

Indexed as

Estrogen Replacement TherapyAcetylationAMP-Activated Protein KinasesAnimalsAortaApoptosisbcl-2-Associated X ProteinCardiomyopathiesChromatin Assembly and DisassemblyDiet, High-FatDisease Models, AnimalEndothelium, VascularEnzyme InhibitorsEstradiolFemaleHistonesAMP-Activated Protein KinasesBax protein, ratbcl-2-Associated X ProteinEnzyme InhibitorsEstradiolHistonesNitric Oxide Synthase Type IIINos3 protein, ratPoly(ADP-ribose) PolymerasesReceptor, Angiotensin, Type 1SIRT1 protein, humanSirtuin 1AMPKpost-menopausal metabolic syndromeSIRT1

Identifiers

PMID23826814
PMCPMC3799593
OpenAlexW1791865091

What Socratic 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 Socratic graph.