TY - JOUR
T1 - Nitric oxide-dependent neovascularization role in the lower extremity disease
AU - Arellano Mendoza, Mónica G.
AU - Robles, Hilda Vargas
AU - Romo, Eunice
AU - Rios, Amelia
AU - Escalante, Bruno
PY - 2007/12
Y1 - 2007/12
N2 - Peripheral arterial occlusive disease (PAD) describes vascular disorders associated with ischemia and PAD affects about 8 million people in the United States. Moreover, PAD's prevalence can increase dramatically if cardiovascular disease is present. In healthy individuals reducing blood flow through the lower extremity is followed by a physiological process to limit ischemia in the distal tissue. This process is called revascularization and impairing revascularization results in PAD. Studies suggest nitric oxide (NO) maybe involved in the ischemia-dependent hindlimb revascularization process. NO is increased in the ischemic hindlimb and eliminating NO impairs the revascularization process. Moreover, restoring NO improves hindlimb revascularization. NO may be acting through its effects on vascular tone, cell migration, or extracellular matrix degradation. The present review illustrates nitric oxide's critical role in the ischemia-induced hindlimb revascularization. Thus, restoring normal NO levels in diseased arteries may represent a viable therapeutic avenue by supplementing exogenous NO or employing therapeutic strategies to either increase NO synthesis and its messengers or decrease NO catabolism.
AB - Peripheral arterial occlusive disease (PAD) describes vascular disorders associated with ischemia and PAD affects about 8 million people in the United States. Moreover, PAD's prevalence can increase dramatically if cardiovascular disease is present. In healthy individuals reducing blood flow through the lower extremity is followed by a physiological process to limit ischemia in the distal tissue. This process is called revascularization and impairing revascularization results in PAD. Studies suggest nitric oxide (NO) maybe involved in the ischemia-dependent hindlimb revascularization process. NO is increased in the ischemic hindlimb and eliminating NO impairs the revascularization process. Moreover, restoring NO improves hindlimb revascularization. NO may be acting through its effects on vascular tone, cell migration, or extracellular matrix degradation. The present review illustrates nitric oxide's critical role in the ischemia-induced hindlimb revascularization. Thus, restoring normal NO levels in diseased arteries may represent a viable therapeutic avenue by supplementing exogenous NO or employing therapeutic strategies to either increase NO synthesis and its messengers or decrease NO catabolism.
KW - Angiogenesis
KW - Arteriogenesis
KW - Nitric oxide
KW - Peripheral arterial disease
KW - Revasculatization
UR - http://www.scopus.com/inward/record.url?scp=36949008535&partnerID=8YFLogxK
U2 - 10.2174/138161207782794103
DO - 10.2174/138161207782794103
M3 - Artículo de revisión
SN - 1381-6128
VL - 13
SP - 3591
EP - 3596
JO - Current Pharmaceutical Design
JF - Current Pharmaceutical Design
IS - 35
ER -