GTP cyclohydrolase I/BH4 pathway protects EPCs via suppressing oxidative stress and thrombospondin-1 in salt-sensitive hypertension.
Endothelial progenitor cells (EPCs) are both reduced and dysfunctional in hypertension that correlates inversely with its mortality, but the mechanisms are poorly understood. Endothelial nitric oxide synthase (eNOS) critically regulates EPC mobilization and function but is uncoupled in salt-sensitiv...
Κύριοι συγγραφείς: | Xie, H, Zhou, S, Chen, D, Channon, K, Su, D, Chen, A |
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Μορφή: | Journal article |
Γλώσσα: | English |
Έκδοση: |
2010
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Παρόμοια τεκμήρια
Παρόμοια τεκμήρια
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GTP cyclohydrolase I/BH4 pathway protects EPCs via suppressing oxidative stress and thrombospondin-1 in salt-sensitive hypertension
ανά: Xie, H, κ.ά.
Έκδοση: (2010) -
GTP Cyclohydrolase/BH4 Pathway Protects EPC Function via Suppressing Oxidative Stress and Thrombospondin-1 in Salt-Sensitive Hypertension
ανά: Xie, H, κ.ά.
Έκδοση: (2009) -
Endothelial-specific GTP cyclohydrolase overexpression reduces blood pressure in salt-sensitive hypertension
ανά: Chen, A, κ.ά.
Έκδοση: (2006) -
GTP cyclohydrolase I prevents diabetic-impaired endothelial progenitor cells and wound healing by suppressing oxidative stress/thrombospondin-1.
ανά: Tie, L, κ.ά.
Έκδοση: (2014) -
BH4 protects endothelial progenitor cell number and function via suppressing thrombospondin-1 expression in salt-sensitive hypertension
ανά: Xie, H, κ.ά.
Έκδοση: (2008)