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NOX signaling in molecular cardiovascular mechanisms involved in the blood pressure homeostasis.

Santillo M, Colantuoni A, Mondola P, Guida B, Damiano S - Front Physiol (2015)

Bottom Line: Blood pressure homeostasis is maintained by several mechanisms regulating cardiac output, vascular resistances, and blood volume.NOXs exert a central role in cardiac mechanosensing, endothelium-dependent relaxation, and Angiotensin-II (Ang-II) redox signaling regulating vascular tone.The central role of NOXs in redox-dependent cardiovascular cell functions renders these enzymes a promising pharmacological target for the treatment of cardiovascular diseases, including hypertension.

View Article: PubMed Central - PubMed

Affiliation: Dipartimento di Medicina Clinica e Chirurgia, Università di Napoli "Federico II" Naples, Italy.

ABSTRACT
Blood pressure homeostasis is maintained by several mechanisms regulating cardiac output, vascular resistances, and blood volume. At cellular levels, reactive oxygen species (ROS) signaling is involved in multiple molecular mechanisms controlling blood pressure. Among ROS producing systems, NADPH oxidases (NOXs), expressed in different cells of the cardiovascular system, are the most important enzymes clearly linked to the development of hypertension. NOXs exert a central role in cardiac mechanosensing, endothelium-dependent relaxation, and Angiotensin-II (Ang-II) redox signaling regulating vascular tone. The central role of NOXs in redox-dependent cardiovascular cell functions renders these enzymes a promising pharmacological target for the treatment of cardiovascular diseases, including hypertension. The aim of the present review is to focus on the physiological role of the cardiovascular NOX-generating ROS in the molecular and cellular mechanisms affecting blood pressure.

No MeSH data available.


Related in: MedlinePlus

NOX isoforms and regulatory subunits. NOX1-4 are associated to the membrane subunit p22phox. NOX4, NOX5, and DUOX1 and 2 do not require cytosolic subunits for their activity. NOX5 and DUOX1 and 2 activation requires Ca2+ binding to their EF-hand domains.
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Figure 1: NOX isoforms and regulatory subunits. NOX1-4 are associated to the membrane subunit p22phox. NOX4, NOX5, and DUOX1 and 2 do not require cytosolic subunits for their activity. NOX5 and DUOX1 and 2 activation requires Ca2+ binding to their EF-hand domains.

Mentions: Up to now, in mammalian, seven different NOX genes (NOX1 to 5 and DUOX1 and 2) have been identified (Lambeth, 2004) (Figure 1). Like NOX2, also NOX1, NOX3, and NOX4 are associated with p22phox, but the mechanisms of activation are different. NOX1 is activated by membrane translocation of the cytosolic subunits NOXO1, NOXA1, and Rac 1or 2, while NOX3 requires NOXO1 but is still uncertain the role of the other cytosolic subunits. NOX4, NOX5, DUOX 1, and 2 activity is not modulated by cytosolic subunits. DUOX 1 and 2 terminate at N-terminus with an extracellular peroxidase-homology domain (PHD) (Donko et al., 2005) and together with NOX5, are modulated by calcium. NOX4 and DUOX1 and 2 produce hydrogen peroxide instead of superoxide anion (Martin et al., 2006).


NOX signaling in molecular cardiovascular mechanisms involved in the blood pressure homeostasis.

Santillo M, Colantuoni A, Mondola P, Guida B, Damiano S - Front Physiol (2015)

NOX isoforms and regulatory subunits. NOX1-4 are associated to the membrane subunit p22phox. NOX4, NOX5, and DUOX1 and 2 do not require cytosolic subunits for their activity. NOX5 and DUOX1 and 2 activation requires Ca2+ binding to their EF-hand domains.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4493385&req=5

Figure 1: NOX isoforms and regulatory subunits. NOX1-4 are associated to the membrane subunit p22phox. NOX4, NOX5, and DUOX1 and 2 do not require cytosolic subunits for their activity. NOX5 and DUOX1 and 2 activation requires Ca2+ binding to their EF-hand domains.
Mentions: Up to now, in mammalian, seven different NOX genes (NOX1 to 5 and DUOX1 and 2) have been identified (Lambeth, 2004) (Figure 1). Like NOX2, also NOX1, NOX3, and NOX4 are associated with p22phox, but the mechanisms of activation are different. NOX1 is activated by membrane translocation of the cytosolic subunits NOXO1, NOXA1, and Rac 1or 2, while NOX3 requires NOXO1 but is still uncertain the role of the other cytosolic subunits. NOX4, NOX5, DUOX 1, and 2 activity is not modulated by cytosolic subunits. DUOX 1 and 2 terminate at N-terminus with an extracellular peroxidase-homology domain (PHD) (Donko et al., 2005) and together with NOX5, are modulated by calcium. NOX4 and DUOX1 and 2 produce hydrogen peroxide instead of superoxide anion (Martin et al., 2006).

Bottom Line: Blood pressure homeostasis is maintained by several mechanisms regulating cardiac output, vascular resistances, and blood volume.NOXs exert a central role in cardiac mechanosensing, endothelium-dependent relaxation, and Angiotensin-II (Ang-II) redox signaling regulating vascular tone.The central role of NOXs in redox-dependent cardiovascular cell functions renders these enzymes a promising pharmacological target for the treatment of cardiovascular diseases, including hypertension.

View Article: PubMed Central - PubMed

Affiliation: Dipartimento di Medicina Clinica e Chirurgia, Università di Napoli "Federico II" Naples, Italy.

ABSTRACT
Blood pressure homeostasis is maintained by several mechanisms regulating cardiac output, vascular resistances, and blood volume. At cellular levels, reactive oxygen species (ROS) signaling is involved in multiple molecular mechanisms controlling blood pressure. Among ROS producing systems, NADPH oxidases (NOXs), expressed in different cells of the cardiovascular system, are the most important enzymes clearly linked to the development of hypertension. NOXs exert a central role in cardiac mechanosensing, endothelium-dependent relaxation, and Angiotensin-II (Ang-II) redox signaling regulating vascular tone. The central role of NOXs in redox-dependent cardiovascular cell functions renders these enzymes a promising pharmacological target for the treatment of cardiovascular diseases, including hypertension. The aim of the present review is to focus on the physiological role of the cardiovascular NOX-generating ROS in the molecular and cellular mechanisms affecting blood pressure.

No MeSH data available.


Related in: MedlinePlus