Journal
CARDIOVASCULAR RESEARCH
Volume 95, Issue 1, Pages 7-18Publisher
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvs143
Keywords
PKA; eNOS; Nitric oxide; Nitrite; Vascular remodelling
Categories
Funding
- ADA Basic Science [1-10-BS-84]
- NIH [HL80482]
- Malcolm Feist Cardiovascular Research Endowment, LSU Health Sciences Center, Shreveport
- National Science Funds of China [81070115, 81170098]
- Major State Basic Research Development Program of China [2012CB945100]
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Although an abundant amount of research has been devoted to the study of angiogenesis, its precise mechanisms are incompletely understood. Numerous clinical trials focused on therapeutic angiogenesis for the treatment of tissue ischaemia have not been as successful as those of preclinical studies. Thus, additional studies are needed to better understand critical molecular mechanisms regulating ischaemic neovascularization to identify novel therapeutic agents. Nitric oxide (NO) plays a central role in ischaemic neovascularization through the generation of cyclic guanosine monophosphate (cGMP) and the activation of several other signalling responses. Accumulated evidence suggests that endothelial protein kinase A/endothelial NO synthase (PKA/eNOS) signalling may play an important role in ischaemic disorders by promoting neovascularization. This review highlights recent advances in the role of the PKA/eNOS and NO-cGMP-kinase cascade pathway in ischaemic neovascularization. We also discuss molecular relationships of PKA/eNOS with other angiogenic pathways and explore the possibility of activation of the NO/nitrite endocrine system as potential therapeutic targets for ischaemic angiogenesis.
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