ReviewCardiology journal2021
Role of extracellular signal-regulated kinase 1/2 signaling underlying cardiac hypertrophy.
Review in Cardiology journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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Who cites it
13 citing papers in PubMed.
- Raf kinase inhibitor protein combined with phosphorylated extracellular signal-regulated kinase offers valuable prognosis in gastrointestinal stromal tumor.World journal of gastroenterology · 2023Trial
- Gastrin ameliorates heart failure and suppresses myocardial remodeling via the JAK2/STAT3 and ERK1/2 pathways.PloS one · 2026Article
- Gestational arsenite exposure alters maternal postpartum heart size and induces CaAmerican journal of physiology. Heart and circulatory physiology · 2025Article
- Ginsenoside Rg1 treats chronic heart failure by downregulating ERK1/2 protein phosphorylation.In vitro cellular & developmental biology. Animal · 2024Article
- RICH1 is a novel key suppressor of isoproterenol‑ or angiotensin II‑induced cardiomyocyte hypertrophy.Molecular medicine reports · 2024Article
- Sex differences in the cardiac stress response following SARS-CoV-2 infection of ferrets.American journal of physiology. Heart and circulatory physiology · 2023Article
- Lithium Treatment Induces Cardiac Dysfunction in Mice.International journal of molecular sciences · 2023Article
- Harnessing RKIP to Combat Heart Disease and Cancer.Cancers · 2022Review
- Guanylyl cyclase-A phosphorylation decreases cardiac hypertrophy and improves systolic function in male, but not female, mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Genome-Wide DNA Methylation Signatures Predict the Early Asymptomatic Doxorubicin-Induced Cardiotoxicity in Breast Cancer.Cancers · 2021Article
- Interactions between the ERK1/2 signaling pathway and PCAF play a key role in PE‑induced cardiomyocyte hypertrophy.Molecular medicine reports · 2021Article
- Silencing ofInternational journal of molecular sciences · 2021Article
- Cardiac Effects of Treadmill Running at Different Intensities in a Rat Model.Frontiers in physiology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy is the result of increased myocardial cell size responding to an increased workload and developmental signals. These extrinsic and intrinsic stimuli as key drivers of cardiac hypertrophy have spurred efforts to target their associated signaling pathways. The extracellular signal-regulated kinases 1/2 (ERK1/2), as an essential member of mitogen-activated protein kinases (MAPKs), has been widely recognized for promoting cardiac growth. Several modified transgenic mouse models have been generated through either affecting the upstream kinase to change ERK1/2 activity, manipulating the direct role of ERK1/2 in the heart, or targeting phosphatases or MAPK scaffold proteins to alter total ERK1/2 activity in response to an increased workload. Using these models, both regulation of the upstream events and modulation of each isoform and indirect effector could provide important insights into how ERK1/2 modulates cardiomyocyte biology. Furthermore, a plethora of compounds, inhibitors, and regulators have emerged in consideration of ERK, or its MAPK kinases, are possible therapeutic targets against cardiac hypertrophic diseases. Herein, is a review of the available evidence regarding the exact role of ERK1/2 in regulating cardiac hypertrophy and a discussion of pharmacological strategy for treatment of cardiac hypertrophy.
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Identifiers
What Socratic holds
Registered trials
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 Socratic graph.