Evidence map›Paper›PMID 32573492›Full record

ArticleThe Journal of clinical investigation2020

p38 Mitogen-activated protein kinase regulates chamber-specific perinatal growth in heart.

Tomohiro Yokota, Jin Li, Jijun Huang, Zhaojun Xiong, Qing Zhang, Tracey Chan, Yichen Ding, Christoph Rau, Kevin Sung, Shuxun Ren and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Python cardiomyocytes store lipids to buffer against hyperlipidemia.Annals of the New York Academy of Sciences · 2025
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  20. p38 MAPK Pathway in the Heart: New Insights in Health and Disease.International journal of molecular sciences · 2020
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 4 countries.

Tomohiro YokotaCardiovascular Research Laboratories, Department of Anesthesiology, Department of Physiology, and Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Jin LiCardiovascular Research Laboratories, Department of Anesthesiology, Department of Physiology, and Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Jijun HuangCardiovascular Research Laboratories, Department of Anesthesiology, Department of Physiology, and Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Zhaojun XiongCardiovascular Research Laboratories, Department of Anesthesiology, Department of Physiology, and Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Qing ZhangIntegrative Biology and Physiology, David Geffen School of Medicine.
Tracey ChanIntegrative Biology and Physiology, David Geffen School of Medicine.
Yichen DingDepartment of Bioengineering, School of Engineering and Applied Sciences.
Christoph RauCardiovascular Research Laboratories, Department of Anesthesiology, Department of Physiology, and Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Kevin SungDepartment of Bioengineering, School of Engineering and Applied Sciences.
Shuxun RenCardiovascular Research Laboratories, Department of Anesthesiology, Department of Physiology, and Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Rajan KulkarniDepartment of Bioengineering, School of Engineering and Applied Sciences.
Tzung HsiaiDepartment of Bioengineering, School of Engineering and Applied Sciences.
Xinshu XiaoIntegrative Biology and Physiology, David Geffen School of Medicine.
Marlin ToumaDepartment of Pediatrics, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
Susumu MinamisawaDepartment of Cell Physiology, Jikei University, Tokyo, Japan.
Yibin WangCardiovascular Research Laboratories, Department of Anesthesiology, Department of Physiology, and Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California, USA.
University of California, Los Angeles · USLaboratoire d’immunologie intégrative du cancer · FRJikei University School of Medicine · JPSun Yat-sen University · CN

Funding

Novel mechanisms in ER regulation in heartR01HL070079 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, YIBIN · 2003 to 2011
$3.2M
Novel Mechanism of SR Calcium Regulation in Cardiac DysfunctionR01HL108186 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, YIBIN · 2011 to 2015
$1.9M
Novel Function and Regulatory Mechanisms of Stress Kinase p38 in HeartR01HL103205 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, YIBIN · 2010 to 2014
$1.9M
Novel Gene-Environment Regulatory Circuit in Chamber-Specific Growth of Perinatal HeartR01HL153853 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TOUMA, MARLIN · 2020 to 2023
$1.6M
A Systems Approach to Uncover Novel Genes and Networks in Heart FailureR21HL110667 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE, WANG, YIBIN · 2011 to 2012
$424k
Novel Gene-Environment Regulatory Circuit in Chamber Specific Growth of Perinatal HeartR56HL146738 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TOUMA, MARLIN · 2019 to 2019
$390k
NHLBI NIH HHS R01 HL070079NHLBI NIH HHS R01 HL103205NHLBI NIH HHS R01 HL108186NHLBI NIH HHS R01 HL153853NHLBI NIH HHS R21 HL110667NHLBI NIH HHS R56 HL146738
6 · The paper itself

Abstract

In the mammalian heart, the left ventricle (LV) rapidly becomes more dominant in size and function over the right ventricle (RV) after birth. The molecular regulators responsible for this chamber-specific differential growth are largely unknown. We found that cardiomyocytes in the neonatal mouse RV had lower proliferation, more apoptosis, and a smaller average size compared with the LV. This chamber-specific growth pattern was associated with a selective activation of p38 mitogen-activated protein kinase (MAPK) activity in the RV and simultaneous inactivation in the LV. Cardiomyocyte-specific deletion of both the Mapk14 and Mapk11 genes in mice resulted in loss of p38 MAPK expression and activity in the neonatal heart. Inactivation of p38 activity led to a marked increase in cardiomyocyte proliferation and hypertrophy but diminished cardiomyocyte apoptosis, specifically in the RV. Consequently, the p38-inactivated hearts showed RV-specific enlargement postnatally, progressing to pulmonary hypertension and right heart failure at the adult stage. Chamber-specific p38 activity was associated with differential expression of dual-specific phosphatases (DUSPs) in neonatal hearts, including DUSP26. Unbiased transcriptome analysis revealed that IRE1α/XBP1-mediated gene regulation contributed to p38 MAPK-dependent regulation of neonatal cardiomyocyte proliferation and binucleation. These findings establish an obligatory role of DUSP/p38/IRE1α signaling in cardiomyocytes for chamber-specific growth in the postnatal heart.

Indexed as

AnimalsAnimals, NewbornApoptosisCell ProliferationCell SizeEnzyme ActivationFemaleGene Expression ProfilingHeartHeart VentriclesMaleMiceMice, KnockoutMitogen-Activated Protein Kinase 14Mitogen-Activated Protein KinasesMyocardiummitogen-activated protein kinase 11, mouseMitogen-Activated Protein Kinase 14Mitogen-Activated Protein KinasesCardiologyEmbryonic developmentHeart failureSignal transduction

Identifiers

PMID32573492
PMCPMC7524480
OpenAlexW3037161372

What OpenQuestion 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 OpenQuestion graph.