ReviewFrontiers in pharmacology2015
Extracellular signal-regulated kinases 1/2 as regulators of cardiac hypertrophy.
Review in Frontiers in pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 96 citations in OpenAlex.
- mTORC1 and nuclear ERK spatially control translation in cardiomyocytes through 4EBP1 phosphorylation.Science signaling · 2026Article
- Integrating Network Pharmacology and In Vitro 3D Cardiac Organoid Model Validation to Investigate the Action Mechanism of Shenfu Xiangshao Decoction on Heart Failure.Journal of cardiovascular pharmacology · 2026Article
- Exploring the Role of Nesprin1 in isoproterenol-induced heart failure: Insights into pathogenesis and therapeutic implications.PloS one · 2026Article
- ETV1 orchestrates a self-reinforcing ERK1/2-RSK3 signaling loop to drive atrial fibrillation pathogenesis: implications for targeted therapy.Scientific reports · 2025Article
- ArfGAP with Dual Pleckstrin Homology Domains 2 Promotes Hypertrophy of Cultured Neonatal Cardiomyocytes.International journal of molecular sciences · 2025Article
- Gut Microbiota and Bacterial Extracellular Vesicles: Emerging Roles in Myocardial Remodelling and Cardiac Health.Journal of extracellular biology · 2025Review
- Polarized macrophages modulate cardiac structure and contractility under hypoxia in novel immuno-heart on a chip.APL bioengineering · 2025Article
- Dual inhibition of TGFβ and PDGF improves RV remodeling and function in response to RV pressure or volume-loading.Physiological reports · 2025Article
- Adiponectin signaling regulates urinary bladder function by blunting smooth muscle purinergic contractility.JCI insight · 2025Article
- The role of ERK1/2 signaling in diabetes: pathogenic and therapeutic implications.Frontiers in pharmacology · 2025Review
- Signalling pathways involved in urotensin II induced ventricular myocyte hypertrophy.PloS one · 2025Article
- Cysteine-Rich Protein 61 (CCN1) Deficiency Alleviated Cardiac Remodeling in 5/6 Nephrectomized Mice by Suppressing the MAPK Signaling Pathway.Cardiovascular therapeutics · 2025Article
- Insights into the Multifaceted Roles of Thioredoxin-1 System: Exploring Knockout Murine Models.Biology · 2024Review
- Exploring TTN variants as genetic insights into cardiomyopathy pathogenesis and potential emerging clues to molecular mechanisms in cardiomyopathies.Scientific reports · 2024Review
- Time-dependent effects of BRAF-V600E on cell cycling, metabolism, and function in engineered myocardium.Science advances · 2024Article
- Role of Mitogen-Activated Protein (MAP) Kinase Pathways in Metabolic Diseases.Genome integrity · 2024Review
- Article
- MEK inhibitors: a promising targeted therapy for cardiovascular disease.Frontiers in cardiovascular medicine · 2024Review
- MEK1-ERK1/2 signaling regulates the cardiomyocyte non-sarcomeric actin cytoskeletal network.American journal of physiology. Heart and circulatory physiology · 2024Article
- LncRNA SNHG8 regulates the migration and angiogenesis of pHUVECs induced by high glucose via the TRPM7/ERKScientific reports · 2023Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy results from increased mechanical load on the heart and through the actions of local and systemic neuro-humoral factors, cytokines and growth factors. These mechanical and neuroendocrine effectors act through stretch, G protein-coupled receptors and tyrosine kinases to induce the activation of a myriad of intracellular signaling pathways including the extracellular signal-regulated kinases 1/2 (ERK1/2). Since most stimuli that provoke myocardial hypertrophy also elicit an acute phosphorylation of the threonine-glutamate-tyrosine (TEY) motif within the activation loops of ERK1 and ERK2 kinases, resulting in their activation, ERKs have long been considered promotors of cardiac hypertrophy. Several mouse models were generated in order to directly understand the causal role of ERK1/2 activation in the heart. These models include direct manipulation of ERK1/2 such as overexpression, mutagenesis or knockout models, manipulations of upstream kinases such as MEK1 and manipulations of the phosphatases that dephosphorylate ERK1/2 such as DUSP6. The emerging understanding from these studies, as will be discussed here, is more complex than originally considered. While there is little doubt that ERK1/2 activation or the lack of it modulates the hypertrophic process or the type of hypertrophy that develops, it appears that not all ERK1/2 activation events are the same. While much has been learned, some questions remain regarding the exact role of ERK1/2 in the heart, the upstream events that result in ERK1/2 activation and the downstream effector in hypertrophy.
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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.