Evidence map›Paper›PMID 40229267›Full record

ArticleCell death & disease2025

β-adrenergic receptor inhibits heart regeneration by downregulating Yap m6A modification.

Kaihang Guan, Zijian Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026
    Review
  2. Review
  3. 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.

Kaihang GuanDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, Beijing Key Laboratory of Cardiovascular Receptors Research, Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Research Unit of Medical Science Research Management/Basic and Clinical Research of Metabolic Cardiovascular Diseases, Chinese Academy of Medical Sciences, Beijing, China.
Zijian LiDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, Beijing Key Laboratory of Cardiovascular Receptors Research, Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Research Unit of Medical Science Research Management/Basic and Clinical Research of Metabolic Cardiovascular Diseases, Chinese Academy of Medical Sciences, Beijing, China. lizijian@bjmu.edu.cn.ORCID http://orcid.org/0000-0002-8057-2257

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82430021, U21A20336, and 81820108031
6 · The paper itself

Abstract

Newborn mammals transiently maintain the heart regenerative capacity. β-adrenergic receptor (β-AR) is the most critical receptor in regulating cardiomyocyte behavior. However, the role and mechanism of β-AR, especially the subtypes of β-AR, in heart regeneration remain unclear. Here, we reveal that β-AR inhibits heart regeneration by downregulating Yap m6A modification. The β-AR expression is associated with heart regenerative capacity. After apical resection, β-AR (including β

Indexed as

Adaptor Proteins, Signal TransducingHeartReceptors, Adrenergic, betaReceptors, Adrenergic, beta-2RegenerationAnimalsCell Cycle ProteinsCell ProliferationDown-RegulationMaleMethyltransferasesMiceMice, Inbred C57BLMyocytes, CardiacYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsMethyltransferasesReceptors, Adrenergic, betaReceptors, Adrenergic, beta-2Yap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID40229267
PMCPMC11997195

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Registered trials

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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.