Evidence map›Paper›PMID 38328937›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2024

p53 Acetylation Exerts Critical Roles in Pressure Overload-Induced Coronary Microvascular Dysfunction and Heart Failure in Mice.

Xiaochen He, Aubrey C Cantrell, Quinesha A Williams, Wei Gu, Yingjie Chen, Jian-Xiong Chen, Heng Zeng

Open access · hybridAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2024. 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
5.7field-weighted citation impact, top 3% 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, 21 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Xiaochen HeDepartment of Physiology and Biophysics (X.H., Y.C.), University of Mississippi Medical Center, School of Medicine, Jackson.ORCID 0000-0002-8266-5895
Aubrey C CantrellDepartment of Pharmacology and Toxicology (A.C.C., Q.A.W., J.-X.C., H.Z.), University of Mississippi Medical Center, School of Medicine, Jackson.ORCID 0000-0002-0686-3443
Quinesha A WilliamsDepartment of Pharmacology and Toxicology (A.C.C., Q.A.W., J.-X.C., H.Z.), University of Mississippi Medical Center, School of Medicine, Jackson.
Wei GuDepartment of Pathology and Cell Biology, Columbia University, Institute for Cancer Genetics, New York, NY (W.G.).
Yingjie ChenDepartment of Physiology and Biophysics (X.H., Y.C.), University of Mississippi Medical Center, School of Medicine, Jackson.ORCID 0000-0002-4059-7847
Jian-Xiong ChenDepartment of Pharmacology and Toxicology (A.C.C., Q.A.W., J.-X.C., H.Z.), University of Mississippi Medical Center, School of Medicine, Jackson.ORCID 0000-0001-9203-4336
Heng ZengDepartment of Pharmacology and Toxicology (A.C.C., Q.A.W., J.-X.C., H.Z.), University of Mississippi Medical Center, School of Medicine, Jackson.ORCID 0000-0001-8559-2807
University of Mississippi Medical Center · USCancer Genetics (United States) · US

Funding

The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI TAYLOR, ERIN BASSFORD · 2013 to 2022
$23.4M
Mechanism of  PD1 on cardiac inflammation resolution during heart failure developmentR01HL161085 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI CHEN, YINGJIE · 2022 to 2025
$2.3M
Endothelial PHD2 in hypertensive vascular remodelingR01HL151536 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI CHEN, JIAN-XIONG · 2021 to 2024
$1.6M
P53 acetylation in microvascular rarefaction and heart failureR56HL164321 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI ZENG, HENG · 2022 to 2022
$388k
NHLBI NIH HHS R01 HL151536NHLBI NIH HHS R01 HL161085NHLBI NIH HHS R56 HL164321NIGMS NIH HHS P20 GM104357
6 · The paper itself

Abstract

backgroundCoronary microvascular dysfunction (CMD) has been shown to contribute to cardiac hypertrophy and heart failure (HF) with preserved ejection fraction. At this point, there are no proven treatments for CMD.

methodsWe have shown that histone acetylation may play a critical role in the regulation of CMD. By using a mouse model that replaces lysine with arginine at residues K98, K117, K161, and K162R of p53 (p53

resultsEchocardiography measurements revealed improved cardiac function together with a reduction of apoptosis and fibrosis in p53

conclusionsOur data reveal the importance of p53 acetylation in coronary microvascular function, cardiac function, and remodeling and may provide a promising approach to improve hypertension-induced CMD and to prevent the transition of cardiac hypertrophy to HF.

Indexed as

Heart FailureHypertensionMyocardial IschemiaAcetylationAnimalsCardiomegalyMiceMice, KnockoutMyocardiumTumor Suppressor Protein p53Tumor Suppressor Protein p53angiogenesiscoronary circulationglycolysisheart failurehypertension

Identifiers

PMID38328937
PMCPMC10978286
OpenAlexW4391651796

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.