Evidence map›Paper›PMID 27575022›Full record

ReviewJournal of molecular and cellular cardiology2016

Regulation of cardiac hypertrophy and remodeling through the dual-specificity MAPK phosphatases (DUSPs).

Ruijie Liu, Jeffery D Molkentin

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 106 citations in OpenAlex.

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  9. Molecular Regulation of Cardiomyocyte Maturation.Current cardiology reports · 2025
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  14. Identification of Oxidative Stress-Related Biomarkers in Diabetic Kidney Disease.Evidence-based complementary and alternative medicine : eCAM · 2022
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  19. Epigenetic Regulation of Autophagy in Cardiovascular Pathobiology.International journal of molecular sciences · 2021
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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 at 2 institutions in 1 country.

Ruijie LiuDepartment of Biomedical Sciences, Grand Valley State University, Allendale, MI 49401, USA; Division of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Jeffery D MolkentinDivision of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA; Howard Hughes Medical Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA. Electronic address: jeff.molkentin@cchmc.org.
Grand Valley State University · USHoward Hughes Medical Institute · US

Funding

MOLECULAR PATHWAYS CONTROLLING CARDIAC GENE EXPRESSIONR01HL060562 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI MOLKENTIN, JEFFERY D · 1998 to 2021
$4.1M
Understanding Cardiovascular Disease MechanismsT32HL125204 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI Evangelia G Kranias, Jeffery D Molkentin · 2015 to 2026
$3.4M
NHLBI NIH HHS R01 HL060562NHLBI NIH HHS T32 HL125204
6 · The paper itself

Abstract

Mitogen-activated protein kinases (MAPKs) play a critical role in regulating cardiac hypertrophy and remodeling in response to increased workload or pathological insults. The spatiotemporal activities and inactivation of MAPKs are tightly controlled by a family of dual-specificity MAPK phosphatases (DUSPs). Over the past 2 decades, we and others have determined the critical role for selected DUSP family members in controlling MAPK activity in the heart and the ensuing effects on ventricular growth and remodeling. More specifically, studies from mice deficient for individual Dusp genes as well as heart-specific inducible transgene-mediated overexpression have implicated select DUSPs as essential signaling effectors in the heart that function by dynamically regulating the level, subcellular and temporal activities of the extracellular signal-regulated kinases (ERKs), c-Jun N-terminal kinases (JNKs) and p38 MAPKs. This review summarizes recent literature on the physiological and pathological roles of MAPK-specific DUSPs in regulating MAPK signaling in the heart and the effect on cardiac growth and remodeling.

Indexed as

Ventricular RemodelingAnimalsCardiomegalyDual-Specificity PhosphatasesHumansIntracellular SpaceIsoenzymesMAP Kinase Signaling SystemMitogen-Activated Protein KinasesProtein TransportDual-Specificity PhosphatasesIsoenzymesMitogen-Activated Protein KinasesCardiac hypertrophyConcentric remodelingDual specificity phosphatasesMitogen-activated protein kinases

Identifiers

PMID27575022
PMCPMC5154921
OpenAlexW2514531847

What OpenQuestion holds

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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.