Evidence map›Paper›PMID 36479975›Full record

ArticleeLife2022

Inhibition of β1-AR/Gαs signaling promotes cardiomyocyte proliferation in juvenile mice through activation of RhoA-YAP axis.

Masahide Sakabe, Michael Thompson, Nong Chen, Mark Verba, Aishlin Hassan, Richard Lu, Mei Xin

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. 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
2.8field-weighted citation impact, top 9% 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, 24 citations in OpenAlex.

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  12. Cardiac maturation.Journal of molecular and cellular cardiology · 2024
    Review
  13. Nucleus Mechanosensing in Cardiomyocytes.International journal of molecular sciences · 2023
    Review
  14. Review
  15. Unlocking cardiomyocyte renewal potential for myocardial regeneration therapy.Journal of molecular and cellular cardiology · 2023
    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

7 authors at 1 institution in 1 country.

Masahide SakabeDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, United States.ORCID 0000-0003-0851-296X
Michael ThompsonDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, United States.
Nong ChenDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, United States.
Mark VerbaDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, United States.
Aishlin HassanDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, United States.
Richard LuDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, United States.
Mei XinDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, United States.ORCID 0000-0002-5732-7501
Cincinnati Children's Hospital Medical Center · US

Funding

Hippo Signaling in Heart Development and RepairR01HL132211 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI XIN, MEI · 2016 to 2020
$1.9M
NHLBI NIH HHS R01 HL132211
6 · The paper itself

Abstract

The regeneration potential of the mammalian heart is incredibly limited, as cardiomyocyte proliferation ceases shortly after birth. β-adrenergic receptor (β-AR) blockade has been shown to improve heart functions in response to injury; however, the underlying mechanisms remain poorly understood. Here, we inhibited β-AR signaling in the heart using metoprolol, a cardio-selective β blocker for β1-adrenergic receptor (β1-AR) to examine its role in heart maturation and regeneration in postnatal mice. We found that metoprolol enhanced cardiomyocyte proliferation and promoted cardiac regeneration post myocardial infarction, resulting in reduced scar formation and improved cardiac function. Moreover, the increased cardiomyocyte proliferation was also induced by the genetic deletion of

Indexed as

Myocytes, CardiacYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCell ProliferationGTP-Binding Protein alpha SubunitsMammalsMetoprololMicerhoA GTP-Binding ProteinAdaptor Proteins, Signal TransducingCell Cycle ProteinsGTP-Binding Protein alpha SubunitsMetoprololrhoA GTP-Binding ProteinYAP-Signaling Proteinsadrenergic signalingcardiomyocyte proliferationdevelopmental biologyhear regenerationhippo pathwaymouse

Identifiers

PMID36479975
PMCPMC9767473
OpenAlexW4311870963

What OpenQuestion 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 OpenQuestion graph.