Evidence map›Paper›PMID 33179140›Full record

ReviewCellular and molecular life sciences : CMLS2021

The regulatory roles of p53 in cardiovascular health and disease.

Hongbo Men, He Cai, Quanli Cheng, Wenqian Zhou, Xiang Wang, Shan Huang, Yang Zheng, Lu Cai

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
5.4field-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

88 citing papers in PubMed, 127 citations in OpenAlex.

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  20. Ubiquitin E3 Ligases and p53 in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2025
    Review

28 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 2 countries.

Hongbo MenDepartment of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, 130021, China.
He CaiDepartment of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, 130021, China.
Quanli ChengDepartment of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, 130021, China.
Wenqian ZhouDepartment of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, 130021, China.
Xiang WangDepartment of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, 130021, China.
Shan HuangDepartment of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, 130021, China.
Yang ZhengDepartment of Cardiovascular Disease, First Hospital of Jilin University, Jilin University, Changchun, 130021, China. zhengyang@jlu.edu.cn.
Lu CaiDepartment of Pediatrics, Pediatric Research Institute, University of Louisville, Louisville, KY, 40202, USA. lu.cai@louisville.edu.ORCID http://orcid.org/0000-0003-3048-1135
University of Louisville · USJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease (CVD) remains the leading cause of mortality globally, so further investigation is required to identify its underlying mechanisms and potential targets for its prevention. The transcription factor p53 functions as a gatekeeper, regulating a myriad of genes to maintain normal cell functions. It has received a great deal of research attention as a tumor suppressor. In the past three decades, evidence has also shown a regulatory role for p53 in the heart. Basal p53 is essential for embryonic cardiac development; it is also necessary to maintain normal heart architecture and physiological function. In pathological cardiovascular circumstances, p53 expression is elevated in both patient samples and animal models. Elevated p53 plays a regulatory role via anti-angiogenesis, pro-programmed cell death, metabolism regulation, and cell cycle arrest regulation. This largely promotes the development of CVDs, particularly cardiac remodeling in the infarcted heart, hypertrophic cardiomyopathy, dilated cardiomyopathy, and diabetic cardiomyopathy. Roles for p53 have also been found in atherosclerosis and chemotherapy-induced cardiotoxicity. However, it has different roles in cardiomyocytes and non-myocytes, even in the same model. In this review, we describe the different effects of p53 in cardiovascular physiological and pathological conditions, in addition to potential CVD therapies targeting p53.

Indexed as

AnimalsCell Cycle CheckpointsCell ProliferationCellular SenescenceDiabetic CardiomyopathiesGene Expression RegulationHumansMyocytes, CardiacSignal TransductionTumor Suppressor Protein p53Tumor Suppressor Protein p53AngiogenesisApoptosisCardiovascular diseaseCell cycle arrestMetabolismp53

Identifiers

PMID33179140
PMCPMC11073000
OpenAlexW3098626916

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.