ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2021
Evolution of β-catenin-independent Wnt-GSK3-mTOR signalling in regulation of energy metabolism in isoproterenol-induced cardiotoxicity model.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Polyherbal Formulation Attenuates Isoproterenol-Induced Cardiac Toxicity Through Regulation of Mitochondrial Bioenergetics, Lipid Toxicity, and Intrinsic Apoptotic Pathways in Rats.Cell biochemistry and biophysics · 2026Article
- Precision Medicine in Colorectal Cancer: Targeted Therapies and Biomarker Insights.Current cancer drug targets · 2026Review
- Microbial oncogenesis: the impact of Fusobacterium nucleatum on oral cancer pathways.Medical oncology (Northwood, London, England) · 2025Review
- DDX3X alleviates doxorubicin-induced cardiotoxicity by regulating Wnt/β-catenin signaling pathway in an in vitro model.Journal of biochemical and molecular toxicology · 2022Article
- Wnt 3a Protects Myocardial Injury in Elderly Acute Myocardial Infarction by Inhibiting Serum Cystatin C/ROS-Induced Mitochondrial Damage.Frontiers in physiology · 2022Article
- Cardioprotective Effects of Aconite in Isoproterenol-Induced Myocardial Infarction in Rats.Oxidative medicine and cellular longevity · 2022Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIsoproterenol (ISO) is widely used agent to study the effects of interventions which could prevent or attenuate the development of myocardial infarction. The sequence of pathological event's revealed that increased myocardial tissue oxygen demand and energy dysregulation exist early during Iso-induced cardiac toxicity. Later, tissue hypoxia results in increased oxidative stress, inflammation and fibrosis along with cardiac dysfunction in this model. The canonical Wnt/β-catenin pathway has been reported to directly implicate in inducing cardiomyocyte hypertrophy and remodelling. However, less is known about the role of non-canonical Wnt signalling in cardiac diseases.
methodCertain evidences have suggested that the activation of Wnt could up-regulate key energy sensor and cell growth regulator mTOR (Mechanistic target of rapamycin) by inhibition of GSK-3β mediator.
resultThe GSK-3β could negatively influence the mTOR activity and produce energy dysregulation during stress or hypoxic conditions. This suggests that the inhibition of GSK-3β by Wnt signalling could up-regulate mTOR levels and thereby restore early myocardial tissue energy balance and prevent cardiac toxicity in rodents.
conclusionWe hereby discuss a novel therapeutic role of the β-catenin independent, Wnt-GSK3-mTOR axis in attenuation of Iso-induced cardiotoxicity in rodents.
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