Reactive oxygen species (ROS) are a byproduct of the normal metabolism of oxygen and have important roles in cell signalling and homeostasis. An imbalance between ROS production and the cellular antioxidant defence system leads to oxidative stress. Environmental factors and genetic interactions play key roles in oxidative stress mediated pathologies. In this paper, we focus on cardiovascular diseases and obesity, disorders strongly related to each other; in which oxidative stress plays a fundamental role. We provide evidence of the key role played by p66(Shc) protein and protein kinase C (PKC) in these pathologies by their intracellular regulation of redox balance and oxidative stress levels. Additionally, we discuss possible therapeutic strategies aimed at attenuating the oxidative damage in these diseases.

Oxidative Stress in Cardiovascular Diseases and Obesity: Role of p66Shc and Protein Kinase C

De Marchi E
Primo
;
Baldassari F
Secondo
;
Bononi A;Wieckowski MR
Penultimo
;
Pinton P.
Ultimo
2013

Abstract

Reactive oxygen species (ROS) are a byproduct of the normal metabolism of oxygen and have important roles in cell signalling and homeostasis. An imbalance between ROS production and the cellular antioxidant defence system leads to oxidative stress. Environmental factors and genetic interactions play key roles in oxidative stress mediated pathologies. In this paper, we focus on cardiovascular diseases and obesity, disorders strongly related to each other; in which oxidative stress plays a fundamental role. We provide evidence of the key role played by p66(Shc) protein and protein kinase C (PKC) in these pathologies by their intracellular regulation of redox balance and oxidative stress levels. Additionally, we discuss possible therapeutic strategies aimed at attenuating the oxidative damage in these diseases.
2013
De Marchi, E; Baldassari, F; Bononi, A; Wieckowski, Mr; Pinton, P.
File in questo prodotto:
File Dimensione Formato  
564961.pdf

accesso aperto

Descrizione: Full text editoriale
Tipologia: Full text (versione editoriale)
Licenza: Creative commons
Dimensione 1.83 MB
Formato Adobe PDF
1.83 MB Adobe PDF Visualizza/Apri

I documenti in SFERA 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/11392/1793106
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 117
  • ???jsp.display-item.citation.isi??? 101
social impact