ArticleBritish journal of pharmacology2011
β₂-Adrenoceptors, NADPH oxidase, ROS and p38 MAPK: another 'radical' road to heart failure?
Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 30 citations in OpenAlex.
- Inhibition of Cardiac p38 Highlights the Role of the Phosphoproteome in Heart Failure Progression.ACS omega · 2025Article
- Promising Therapeutic Treatments for Cardiac Fibrosis: Herbal Plants and Their Extracts.Cardiology and therapy · 2023Review
- Screening and identification of effective components from modified Taohong Siwu decoction for protecting H9c2 cells from damage.In vitro cellular & developmental biology. Animal · 2023Article
- Takotsubo Syndrome: Translational Implications and Pathomechanisms.International journal of molecular sciences · 2022Review
- Influence of Heat Stress on Intestinal Epithelial Barrier Function, Tight Junction Protein, and Immune and Reproductive Physiology.BioMed research international · 2022Review
- Ibogaine-Mediated ROS/Antioxidant Elevation in Isolated Rat Uterus Is β-Adrenergic Receptors and KAntioxidants (Basel, Switzerland) · 2021Article
- Involvement of Histamine 2 Receptor in Alpha 1 Adrenoceptor Mediated Cardiac Hypertrophy and Oxidative Stress in H9c2 Cardio Myoblasts.Journal of cardiovascular translational research · 2021Article
- Lack of Contribution of p66shc to Pressure Overload-Induced Right Heart Hypertrophy.International journal of molecular sciences · 2020Article
- Cysteine redox state regulates human β2-adrenergic receptor binding and function.Scientific reports · 2020Article
- Beneficial effects of benfotiamine, a NADPH oxidase inhibitor, in isoproterenol-induced myocardial infarction in rats.PloS one · 2020Article
- Improved heart failure by Rhein lysinate is associated with p38MAPK pathway.Experimental and therapeutic medicine · 2018Article
- Aspirin alleviates cardiac fibrosis in mice by inhibiting autophagy.Acta pharmacologica Sinica · 2017Article
- Xanthohumol Modulates Calcium Signaling in Rat Ventricular Myocytes: Possible Antiarrhythmic Properties.The Journal of pharmacology and experimental therapeutics · 2017Article
- Effects of β-adrenoceptor subtypes on cardiac function in myocardial infarction rats exposed to fine particulate matter (PM 2.5).BioMed research international · 2014Article
- Proteomic analysis identifies an NADPH oxidase 1 (Nox1)-mediated role for actin-related protein 2/3 complex subunit 2 (ARPC2) in promoting smooth muscle cell migration.International journal of molecular sciences · 2013Article
- Peroxisome-proliferator-activated receptors regulate redox signaling in the cardiovascular system.World journal of cardiology · 2013Article
- TAK1 activates AMPK-dependent cell death pathway in hydrogen peroxide-treated cardiomyocytes, inhibited by heat shock protein-70.Molecular and cellular biochemistry · 2013Article
- Adrenergic signaling and oxidative stress: a role for sirtuins?Frontiers in physiology · 2013Review
- H(2)O (2)-induced secretion of tumor necrosis factor-α evokes apoptosis of cardiac myocytes through reactive oxygen species-dependent activation of p38 MAPK.Cytotechnology · 2012Article
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3 authors at 2 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Persistent activation of the cardiac β-adrenergic system may contribute to the pathogenesis of congestive heart failure. Both β₁- and β₂-adrenoceptors are known to mediate these noxious effects, yet the β₁-adrenoceptor-PKA axis has received greater attention with less information available on β₂-adrenoceptor driven pathways. In the present issue, Xu and colleagues provide new evidence, showing that β₂-adrenoceptor over-expression leads to increased reactive oxygen species (ROS) emission, mainly caused by up-regulation of reduced nicotinamide adenine dinucleotide phosphate oxidase (Nox) 2 and 4. Increase in ROS levels is accompanied by p38 mitogen-activated protein kinase activation, fibrosis, apoptosis and cardiac dysfunction. Both Nox inhibition and administration of the antioxidant N-acetyl cysteine prevent these adverse effects. Interestingly, antioxidant treatment also prevents the increase in Nox expression, suggesting that β₂-adrenoceptor stimulation triggers a vicious cycle eventually amplified by both Nox isoforms. The possible existence of a circuitry to enhance ROS signalling and detrimental consequences on myocardial remodelling are also discussed, in light of the recent description of intracellular localization of Nox4.
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