Cardiovascular diseases are the main cause of mortality and morbidity in the world. Hypertension, ischemia/reperfusion, diabetes and anti-cancer drugs contribute to heart failure through oxidative and nitrosative stresses which cause cardiomyocytes nuclear and mitochondrial DNA damage, denaturation of intracellular proteins, lipid peroxidation and inflammation. Oxidative or nitrosative stress-mediated injury lead to cardiomyocytes apoptosis or necrosis. The reactive oxygen (ROS) and nitrogen species (RNS) concentration is dependent on their production and on the expression and activity of anti-oxidant enzymes. Polyphenols are a large group of natural compounds ubiquitously expressed in plants, and epidemiological studies have shown associations between a diet rich in polyphenols and the prevention of various ROS-mediated human diseases. Polyphenols reduce cardiomyocytes damage, necrosis, apoptosis, infarct size and improve cardiac function by decreasing oxidative stress-induced production of ROS or RNS. These effects are achieved by the ability of polyphenols to modulate the expression and activity of anti-oxidant enzymes and several signaling pathways involved in cells survival. This report reviews current knowledge on the potential anti-oxidative effects of polyphenols to control the cardiotoxicity induced by ROS and RNS stress.

Mattera, R., Benvenuto, M., Giganti, M.g., Tresoldi, I., Pluchinotta, F., Bergante, S., et al. (2017). Effects of polyphenols on oxidative stress-mediated injury in cardiomyocytes. NUTRIENTS, 9(5), 523 [10.3390/nu9050523].

Effects of polyphenols on oxidative stress-mediated injury in cardiomyocytes

Benvenuto, M;GIGANTI, MARIA GABRIELLA;TRESOLDI, ILARIA;MANZARI, VITTORIO;MODESTI, ANDREA;BEI, ROBERTO
2017-01-01

Abstract

Cardiovascular diseases are the main cause of mortality and morbidity in the world. Hypertension, ischemia/reperfusion, diabetes and anti-cancer drugs contribute to heart failure through oxidative and nitrosative stresses which cause cardiomyocytes nuclear and mitochondrial DNA damage, denaturation of intracellular proteins, lipid peroxidation and inflammation. Oxidative or nitrosative stress-mediated injury lead to cardiomyocytes apoptosis or necrosis. The reactive oxygen (ROS) and nitrogen species (RNS) concentration is dependent on their production and on the expression and activity of anti-oxidant enzymes. Polyphenols are a large group of natural compounds ubiquitously expressed in plants, and epidemiological studies have shown associations between a diet rich in polyphenols and the prevention of various ROS-mediated human diseases. Polyphenols reduce cardiomyocytes damage, necrosis, apoptosis, infarct size and improve cardiac function by decreasing oxidative stress-induced production of ROS or RNS. These effects are achieved by the ability of polyphenols to modulate the expression and activity of anti-oxidant enzymes and several signaling pathways involved in cells survival. This report reviews current knowledge on the potential anti-oxidative effects of polyphenols to control the cardiotoxicity induced by ROS and RNS stress.
2017
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore MED/04 - PATOLOGIA GENERALE
English
cardiomyocytes; cardiovascular disease; oxidative stress; polyphenols
Mattera, R., Benvenuto, M., Giganti, M.g., Tresoldi, I., Pluchinotta, F., Bergante, S., et al. (2017). Effects of polyphenols on oxidative stress-mediated injury in cardiomyocytes. NUTRIENTS, 9(5), 523 [10.3390/nu9050523].
Mattera, R; Benvenuto, M; Giganti, Mg; Tresoldi, I; Pluchinotta, F; Bergante, S; Tettamanti, G; Masuelli, L; Manzari, V; Modesti, A; Bei, R
Articolo su rivista
File in questo prodotto:
File Dimensione Formato  
nutrients-09-00523.pdf

accesso aperto

Tipologia: Versione Editoriale (PDF)
Licenza: Creative commons
Dimensione 1.37 MB
Formato Adobe PDF
1.37 MB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/183247
Citazioni
  • ???jsp.display-item.citation.pmc??? 42
  • Scopus 90
  • ???jsp.display-item.citation.isi??? 82
social impact