(2001). Impaired collateral vessel development in diabetes: potential cellular mechanisms and therapeutic implications.
(2009). Increased expression of CXCR4 and integrin alphaM in hypoxia-preconditioned cells contributes to improved cell retention and angiogenic potency.
(2005). International union of pharmacology. XLV. Classification of the kinin receptor family: from molecular mechanisms to pathophysiological consequences.
(2004). Mobilization of CD34/CXCR4+, CD34/CD117+, c-met+ stem cells, and mononuclear cells expressing early cardiac, muscle, and endothelial markers into peripheral blood in patients with acute myocardial infarction.
(2009). Molecular control of blood flow and angiogenesis: role of nitric oxide.
(2006). Nitric oxide cytoskeletal-induced alterations reverse the endothelial progenitor cell migratory defect associated with diabetes.
(1997). Nitric oxide inactivates NADPH oxidase in pig neutrophils by inhibiting its assembling process.
(2007). Nitric oxide suppresses NADPH oxidase-dependent superoxide production by S-nitrosylation in human endothelial cells. Cardiovasc Res.75:
(2009). NOX and inflammation in the vascular adventitia.
(2006). Number and function of endothelial progenitor cells as a marker of severity for diabetic vasculopathy.
(2007). Oxidant stress impairs in vivo reendothelialization capacity of endothelial progenitor cells from patients with type 2 diabetes mellitus: restoration by the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone.
(2008). Participation of kallikrein-kinin system in different pathologies.
(2008). Role of kinin B2 receptor signaling in the recruitment of circulating progenitor cells with neovascularization potential.
(2008). Spatiotemporal regulation of ERK2 by dual-specificity phosphatases.
(2002). Targeting kinin B(1) receptor for therapeutic neovascularization.
(2009). The definition of EPCs and other bone marrow cells contributing to neoangiogenesis and tumor growth: Is there common ground for understanding the roles of numerous marrow-derived cells in the neoangiogenic process?
(2005). Transgenic activation of the kallikrein-kinin system inhibits intramyocardial inflammation, endothelial dysfunction and oxidative stress in experimental diabetic cardiomyopathy.