Evidence map›Paper›PMID 39892959›Full record

ArticleJournal of molecular and cellular cardiology2025

Dual inhibition of Mst1 and Mst2 exacerbates cardiac dysfunction during pressure overload stress in mice.

Jin Guan, Nadezhda Fefelova, Peiyong Zhai, Yoshiyuki Ikeda, Takanobu Yamamoto, Satvik Mareedu, Jamie Francisco, Lai-Hua Xie, Dae-Sik Lim, Dominic P Del Re

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of molecular and cellular cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Dysfunctional cardiomyocyte signalling and heart disease.Current opinion in cell biology · 2025
    Review
  3. Review
  4. Article
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

10 authors.

Jin GuanDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, USA.
Nadezhda FefelovaDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, USA.
Peiyong ZhaiDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, USA.
Yoshiyuki IkedaDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, USA.
Takanobu YamamotoDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, USA.
Satvik MareeduDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, USA.
Jamie FranciscoDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, USA.
Lai-Hua XieDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, USA.
Dae-Sik LimDepartment of Biological Sciences, National Creative Research Initiatives Center, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea.
Dominic P Del ReDepartment of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, USA. Electronic address: delredo@njms.rutgers.edu.

Funding

The role of Neurofibromin 2 in heart failureR01HL157483 · NHLBI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI Dominic P Del Re · 2022 to 2026
$2.9M
The role of NF2 in myocardial ischemia and reperfusion injuryR01HL127339 · NHLBI · RBHS-NEW JERSEY MEDICAL SCHOOL · PI DEL RE, DOMINIC P · 2015 to 2019
$2.0M
NHLBI NIH HHS R01 HL127339NHLBI NIH HHS R01 HL157483
6 · The paper itself

Abstract

Heart failure remains a leading cause of morbidity and mortality worldwide. The evolutionarily conserved Hippo-Yap signaling pathway regulates cardiac responses to stress and progression to heart failure. Mst1 and Mst2 are the core Hippo pathway kinases, yet their role within chronically stressed cardiomyocytes remains largely unknown. Genetic mouse models revealed that the extent of Mst1/2 inhibition elicits opposing effects on stress-induced cardiac dysfunction. Yap-TEAD1 activation, cell cycling, and hallmarks of cardiomyocyte dedifferentiation, which can impair contractile function during sustained stress, were enhanced in Mst1/2 double knockout hearts. These findings implicate a physiological function of Mst1/2 to promote cardiomyocyte maturity in the adult heart.

Indexed as

Heart FailureHepatocyte Growth FactorProtein Serine-Threonine KinasesStress, PhysiologicalAdaptor Proteins, Signal TransducingAnimalsDisease Models, AnimalHippo KinasesMiceMice, KnockoutMyocytes, CardiacProto-Oncogene ProteinsSerine-Threonine Kinase 3Signal TransductionYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingHepatocyte Growth FactorHippo Kinasesmacrophage stimulating proteinProtein Serine-Threonine KinasesProto-Oncogene ProteinsSerine-Threonine Kinase 3Stk3 protein, mouseStk4 protein, mouseYap1 protein, mouseYAP-Signaling ProteinsCardiac hypertrophyCardiomyocyteCardiovascular diseaseHeart failureHippo-YapSignal transduction

Identifiers

PMID39892959
PMCPMC13138688

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.