A., Figueroa, A., Navaei, N., Wong, A., Kalfon, R., Ormsbee, L.
Polyphenols and human health: Prevention of disease and mechanisms of action. Vauzour, D., Rodriguez-Mateos, A., Corona, G., Oruna-Concha, M. The American Journal of Clinical Nutrition, 81(1), 317S–325S. Polyphenols and disease risk in epidemiologic studies 1–4. Geneva: World Health Organization in collaboration with the World Heart Federation and the World Stroke Organization.Īrts, I. Global Atlas on cardiovascular disease prevention and control. Isoproterenol cytotoxicity is dependent on the differentiation state of the cardiomyoblast H9c2 cell line. International Journal of Biochemistry and Cell Biology, 45(11), 2379–2391.īranco, A. Mitochondrial disruption occurs downstream from β-adrenergic overactivation by isoproterenol in differentiated, but not undifferentiated H9c2 cardiomyoblasts: Differential activation of stress and survival pathways. Increased energy demand during adrenergic receptor stimulation contributes to Ca 2+ wave generation. Reactive oxygen species contribute to the development of arrhythmogenic Ca 2+ waves during β-adrenergic receptor stimulation in rabbit cardiomyocytes. Beta-adrenergic enhancement of sarcoplasmic reticulum calcium leak in cardiac myocytes is mediated by calcium/calmodulin-dependent protein kinase. Mitochondrial production of reactive oxygen species contributes to the β-adrenergic stimulation of mouse cardiomycytes. C., Fauconnier, J., Yamada, T., Lacampagne, A., Zhang, S.-J., Katz, A., et al. β-Adrenergic stimulation and myocardial function in the failing heart. European Journal of Clinical Investigation, 46(4), 362–374.Įl-Armouche, A., & Eschenhagen, T. β-Adrenergic receptor signalling and its functional consequences in the diseased heart. Calcium cycling and signaling in cardiac myocytes. Pflugers Archiv European Journal of Physiology, 466(6), 1139–1150.īers, D. Adrenergic signaling in heart failure: A balance of toxic and protective effects. These metabolites modulate cardiomyocyte beating and Ca 2+ transients following β-adrenergic prolonged stimulation.īaker, A. Unexpected cardioprotective properties of the recently identified human-circulating berry-derived polyphenol metabolites were identified. Finally, phenolic metabolites also prevented ISO-increased activation of PKA–cAMP pathway, modulating Ca 2+ signalling and rescuing cells from an arrhythmogenic Ca 2+ transients’ phenotype. Likewise, phenolic metabolites increased cell beating rate and synchronized cardiomyocyte beating population, following prolonged β-adrenergic receptor activation. The presence of phenolic metabolites limited ISO-induced mitochondrial oxidative stress. Cardiomyocytes were then challenged with the β-adrenergic agonist isoproterenol (ISO) for 24 h. The experimental conditions mimic the physiological concentrations and circulating time of these metabolites in the human plasma (2 h). Ventricular cardiomyocytes derived from neonate rats were treated with three human bioavailable phenolic metabolites found in circulating human plasma, following berries’ ingestion (catechol- O-sulphate, pyrogallol- O-sulphate, and 1-methylpyrogallol- O-sulphate). Herein the cardioprotective effect of human metabolites derived from polyphenols present in berries was assessed in cardiomyocytes, in response to chronic β-adrenergic stimulation, to disclose some of the underlying molecular mechanisms. Nevertheless, chronic activation of β-adrenergic receptors can cause arrhythmias, oxidative stress and cell death. Physiological β-adrenergic stimulation promotes beneficial inotropic effects by increasing heart rate, contractility and relaxation speed of cardiomyocytes.
Thus, diet plays a key role in CVD development and/or prevention. Several epidemiological studies and experimental approaches have demonstrated that consumption of polyphenol-enriched fruits and vegetables can promote cardioprotection. Cardiovascular disease (CVD) is a public health concern, and the third cause of death worldwide.