Activation of Nrf2/HO-1 Pathway and Human Atherosclerotic Plaque Vulnerability:an In Vitro and In Vivo Study

Cells

29 April Apr 2019 26 days ago
  • Fiorelli S, Porro B, Cosentino N, Di Minno A, Manega CM, Fabbiocchi F, Barbieri S, Marenzi G, Cavalca V, Tremoli E, Eligini S.

Reactive oxygen species (ROS) induce nuclear factor erythroid 2-related factor 2 (Nrf2) activation as an adaptive defense mechanism, determining the synthesis of antioxidant molecules, including heme-oxygenase-1 (HO-1). HO-1 protects cells against oxidative injury, degrading free heme and inhibiting ROS production. HO-1 is highly expressed in macrophages during plaque growth. Macrophages are morpho-functionally heterogeneous, and the prevalence of a specific phenotype may influence the plaque fate. This heterogeneity has also been observed in monocyte-derived macrophages (MDMs), a model of macrophages infiltrating tissue. The study aims to assess oxidative stress status and Nrf2/HO-1 axis in MDM morphotypes obtained from healthy subjects and coronary artery disease (CAD) patients, in relation to coronary plaque features evaluated in vivo by optical coherence tomography (OCT).

Reference

Fiorelli S, Porro B, Cosentino N, Di Minno A, Manega CM, Fabbiocchi F, Niccoli G, Fracassi F, Barbieri S, Marenzi G, Crea F, Cavalca V, Tremoli E, Eligini S. Activation of Nrf2/HO-1 Pathway and Human Atherosclerotic Plaque Vulnerability:an In Vitro and In Vivo Study. Cells 2019 Apr 16;8(4). pii: E356. doi: 10.3390/cells8040356.

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