Abstract
| Lingua originale | English |
|---|---|
| pagine (da-a) | 2230-2237 |
| Numero di pagine | 8 |
| Rivista | Frontiers in Bioscience |
| Volume | 14 |
| Stato di pubblicazione | Published - 2009 |
Fingerprint
All Science Journal Classification (ASJC) codes
- Biochemistry, Genetics and Molecular Biology(all)
- Immunology and Microbiology(all)
Cita questo
Role of oxidative and nitrosative stress biomarkers in chronic heart failure. / Zummo, Giovanni; La Rocca, Giampiero; Anzalone, Rita; Magno, Francesca; Carbone, Marco; Gnemmi, Isabella; Eleuteri, Ermanno; Magno, Francesca; Colombo, Marilena; Di Stefano, Antonino; Genta, Francesco Tarro; Giannuzzi, Pantaleo; Carbone, Marco.
In: Frontiers in Bioscience, Vol. 14, 2009, pag. 2230-2237.Risultato della ricerca: Article
}
TY - JOUR
T1 - Role of oxidative and nitrosative stress biomarkers in chronic heart failure
AU - Zummo, Giovanni
AU - La Rocca, Giampiero
AU - Anzalone, Rita
AU - Magno, Francesca
AU - Carbone, Marco
AU - Gnemmi, Isabella
AU - Eleuteri, Ermanno
AU - Magno, Francesca
AU - Colombo, Marilena
AU - Di Stefano, Antonino
AU - Genta, Francesco Tarro
AU - Giannuzzi, Pantaleo
AU - Carbone, Marco
PY - 2009
Y1 - 2009
N2 - In this review, we present recent insights on chronic heart failure (CHF) and the potential role of tumor necrosis factor (TNF)-alpha, interleukins, myeloperoxidase (MPO), and nitrosative stress in the progression of this disease process. Reactive oxygen species (ROS) are produced as a consequence of aerobic metabolism. Under physiologic conditions, their unfavourable effect in causing oxidative damage is counteracted by antioxidants. An imbalance in favour of oxidants leads to oxidative stress, and contributes to myocyte apoptosis, direct negative inotropic effects, and reduced bioavailability of nitric oxide (NO). Together, these effects lead to impaired vasodilatation of the coronary, pulmonary and peripheral vascular beds. In patients with moderate to severe forms of CHF, TNF-alpha leads to the formation of nitrotyrosine and consumption of nitric oxide by virtue of activation of myeloperoxidase. Further studies are required to better elucidate the complex interaction of oxidative stress, endothelial dysfunction and inflammatory activation in CHF. Such insights would likely lead to development of better strategies for the assessment of the disease severity by monitoring of new bio-humoral indices and better treatment approaches.
AB - In this review, we present recent insights on chronic heart failure (CHF) and the potential role of tumor necrosis factor (TNF)-alpha, interleukins, myeloperoxidase (MPO), and nitrosative stress in the progression of this disease process. Reactive oxygen species (ROS) are produced as a consequence of aerobic metabolism. Under physiologic conditions, their unfavourable effect in causing oxidative damage is counteracted by antioxidants. An imbalance in favour of oxidants leads to oxidative stress, and contributes to myocyte apoptosis, direct negative inotropic effects, and reduced bioavailability of nitric oxide (NO). Together, these effects lead to impaired vasodilatation of the coronary, pulmonary and peripheral vascular beds. In patients with moderate to severe forms of CHF, TNF-alpha leads to the formation of nitrotyrosine and consumption of nitric oxide by virtue of activation of myeloperoxidase. Further studies are required to better elucidate the complex interaction of oxidative stress, endothelial dysfunction and inflammatory activation in CHF. Such insights would likely lead to development of better strategies for the assessment of the disease severity by monitoring of new bio-humoral indices and better treatment approaches.
UR - http://hdl.handle.net/10447/40936
UR - http://www.bioscience.org/2009/v14/af/3375/fulltext.asp?bframe=3.htm&doi=yes
M3 - Article
VL - 14
SP - 2230
EP - 2237
JO - Frontiers in Bioscience - Landmark
JF - Frontiers in Bioscience - Landmark
SN - 1093-9946
ER -