ArticleThe journal of physiological sciences : JPS2018
Investigating β-adrenergic-induced cardiac hypertrophy through computational approach: classical and non-classical pathways.
Article in The journal of physiological sciences : JPS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 32 citations in OpenAlex.
- Geraniin attenuates isoproterenol-induced cardiac hypertrophy by inhibiting inflammation, oxidative stress and cellular apoptosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Status of βReviews in cardiovascular medicine · 2023Review
- Regulation of cardiac function by cAMP nanodomains.Bioscience reports · 2023Review
- Cardiac Function in Children and Young Adults Treated with MEK Inhibitors: A Retrospective Cohort Study.Pediatric cardiology · 2022Article
- Effect of cardioplegic arrest and reperfusion on left and right ventricular proteome/phosphoproteome in patients undergoing surgery for coronary or aortic valve disease.International journal of molecular medicine · 2022Article
- Review of applications and challenges of quantitative systems pharmacology modeling and machine learning for heart failure.Journal of pharmacokinetics and pharmacodynamics · 2022Review
- Shexiang Baoxin Pills Could Alleviate Isoproterenol-Induced Heart Failure Probably through its Inhibition of CaV1.2 Calcium Channel Currents.Biochemistry research international · 2022Article
- Review
- Temporal pattern and synergy influence activity of ERK signaling pathways during L-LTP induction.eLife · 2021Article
- The stimulation and inhibition of beta-2 adrenergic receptor on the inflammatory responses of ovary and immune system in the aged laying hens.BMC veterinary research · 2021Article
- Activation of βArchives of pharmacal research · 2021Review
- β-arrestin2 regulating β2-adrenergic receptor signaling in hepatic stellate cells contributes to hepatocellular carcinoma progression.Journal of Cancer · 2021Article
- Context-specific network modeling identifies new crosstalk in β-adrenergic cardiac hypertrophy.PLoS computational biology · 2020Article
- Clinical value of detecting autoantibodies against βJournal of geriatric cardiology : JGC · 2020Article
- Clinical-pathological correlations of BAV and the attendant thoracic aortopathies. Part 2: Pluridisciplinary perspective on their genetic and molecular origins.Journal of molecular and cellular cardiology · 2019Review
- Calcium Sensing Receptor-Related Pathway Contributes to Cardiac Injury and the Mechanism of Astragaloside IV on Cardioprotection.Frontiers in pharmacology · 2018Article
- Wogonin Attenuates Isoprenaline-Induced Myocardial Hypertrophy in Mice by Suppressing the PI3K/Akt Pathway.Frontiers in pharmacology · 2018Article
- Shexiang Tongxin dropping pill protects against isoproterenol-induced myocardial ischemiaOncotarget · 2017Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The chronic stimulation of β-adrenergic receptors plays a crucial role in cardiac hypertrophy and its progression to heart failure. In β-adrenergic signaling, in addition to the well-established classical pathway, Gs/AC/cAMP/PKA, activation of non-classical pathways such as Gi/PI3K/Akt/GSK3β and Gi/Ras/Raf/MEK/ERK contribute in cardiac hypertrophy. The signaling network of β-adrenergic-induced hypertrophy is very complex and not fully understood. So, we use a computational approach to investigate the dynamic response and contribution of β-adrenergic mediators in cardiac hypertrophy. The proposed computational model provides insights into the effects of β-adrenergic classical and non-classical pathways on the activity of hypertrophic transcription factors CREB and GATA4. The results illustrate that the model captures the dynamics of the main signaling mediators and reproduces the experimental observations well. The results also show that despite the low portion of β2 receptors out of total cardiac β-adrenergic receptors, their contribution in the activation of hypertrophic mediators and regulation of β-adrenergic-induced hypertrophy is noticeable and variations in β1/β2 receptors ratio greatly affect the ISO-induced hypertrophic response. The model results illustrate that GSK3β deactivation after β-adrenergic receptor stimulation has a major influence on CREB and GATA4 activation and consequent cardiac hypertrophy. Also, it is found through sensitivity analysis that PKB (Akt) activation has both pro-hypertrophic and anti-hypertrophic effects in β-adrenergic signaling.
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