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Cited by 127Protein Kinase Regulation and GTPase SignalingCardiac Fibrosis and RemodelingProtein Tyrosine Phosphatases

p38 MAP kinases in the heart

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Yokota, Tomohiro, Wang, Yibin·2016·Gene
DOI 10.1016/j.gene.2015.09.030PMC PMC4860190
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Abstract

p38 kinases are members of the mitogen-activated protein kinases (MAPK) with established contribution to a wide range of signaling pathways and different biological processes. The prototypic p38 MAPK, p38α was originally identified as an essential signaling kinase for inflammatory cytokine production Extensive studies have now revealed that p38s have critical roles in many different tissues far beyond immune regulation and inflammatory responses. In this review, we will focus on the structure and molecular biology of p38s, and their specific roles in heart, especially regarding myocyte proliferation, apoptosis, and hypertrophic responses.

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  • PKC might induce p38 MAPK-mediated inactivation of AKTs, proteins essential for DAT cell surface redistribution due to AKT induction of actin reorganization, regulating the dopamine efflux impaired in ADHD.

    “In addition, PKC might induce p38 MAPK-mediated inactivation of AKTs [184, 185], proteins essential for DAT cell surface redistribution due to AKT induction of actin reorganization, regulating the dopamine efflux impaired in ADHD [186].”

    From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [185]

    Section 4.2, “Apoptotic roles in the heart” (page unavailable), reports that p38 MAPK activation can lead to AKT inactivation in cardiomyocytes. It attributes that activation to chronic insulin exposure and metabolic stress, not PKC. The later DAT and dopamine-efflux clause is separately cited to [186], so it is not assessed here. (LLM, conf=0.85)

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Cited by

Sorted by citations

Authors
Yokota, T., & Wang, Y.
Affiliations
University of California, Los Angeles (US)
Corresponding author
Wang, Yibin
ORCID
Venue
Gene
Publisher
Elsevier BV
Published
2016-01
Volume
575
Issue
2
Pages
369-376
ISSN
0378-1119 (ISSN-L)
DOI
10.1016/j.gene.2015.09.030
PMC
PMC4860190
OpenAlex
W1813955311
Cited by
127
References
2
Citations by year
2026: 3 · 2025: 10 · 2024: 10 · 2023: 7 · 2022: 14 · 2021: 18 · 2020: 20 · 2019: 13 · 2018: 10 · 2017: 14 · 2016: 7 · 2015: 1
FWCI
1.03
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Gene (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
NHLBI (HL070079, HL108186, HL103205)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
Keywords
p38 MAPK, p38α, heart, cardiomyocytes, myocyte proliferation, apoptosis, cardiac hypertrophy, MAPK signaling
MeSH terms
Animals, Cardiomegaly, Humans, Myocardium, Apoptosis, MAP Kinase Signaling System, Myocytes, Cardiac, p38 Mitogen-Activated Protein Kinases, Cell Proliferation

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