• Publications
  • Influence
Formation of Isoprostane-like Compounds (Neuroprostanes) in Vivo from Docosahexaenoic Acid*
TLDR
F4-neuroprostane-containing aminophospholipids might adversely effect neuronal function as a result of alterations they induce in the biophysical properties of neuronal membranes, and may provide a unique marker of oxidative injury to the brain and could potentially exert biological activity. Expand
Retinopathy of prematurity: understanding ischemic retinal vasculopathies at an extreme of life.
TLDR
Current concepts on retinal microvascular degeneration, neovascularization, and available treatments, as well as present future perspectives toward more profound elucidation of the pathogenesis of ROP are discussed. Expand
The succinate receptor GPR91 in neurons has a major role in retinal angiogenesis
TLDR
It is shown that succinate accumulates in the hypoxic retina of rodents and, via its cognate receptor G protein–coupled receptor-91 (GPR91), is a potent mediator of vessel growth in the settings of both normal retinal development and proliferative ischemic retinopathy. Expand
Hypoxia Up-regulates CD36 Expression and Function via Hypoxia-inducible Factor-1- and Phosphatidylinositol 3-Kinase-dependent Mechanisms*
TLDR
A novel mechanism by which hypoxia induces CD36 expression via activation of HIF-1 and the phosphatidylinositol 3-kinase pathway is indicated. Expand
Choroidal involution is a key component of oxygen-induced retinopathy.
TLDR
It is demonstrated for the first time pronounced, sustained choroidal vascular involution during the development of ROP, and foundings suggest that effective therapeutic strategies to counter ROP should consider choroid preservation. Expand
Oxidants, nitric oxide and prostanoids in the developing ocular vasculature: a basis for ischemic retinopathy.
TLDR
This review focuses on the important and complex interaction between prostanoid, NO and peroxidation products on circulatory control of the immature retina. Expand
New insights into the retinal circulation: inflammatory lipid mediators in ischemic retinopathy.
TLDR
This review focuses on mechanisms that precede the development of neovascularization, most notably regarding the role of lipid mediators that partake in microvascular degeneration. Expand
Microglia and Interleukin-1&bgr; in Ischemic Retinopathy Elicit Microvascular Degeneration Through Neuronal Semaphorin-3A
TLDR
It is suggested that in the early stages of O2-induced retinopathy, retinal microglia are activated to produce IL-1&bgr;, which sustains the activation ofmicroglia and induces microvascular injury through the release of Sema3A from adjacent neurons. Expand
Ghrelin modulates physiologic and pathologic retinal angiogenesis through GHSR-1a.
TLDR
It is suggested that the ghrelin-GHSR-1a pathway can exert opposing effects on retinal vasculature, depending on the phase of retinopathy, and thus holds therapeutic potential for proliferative retinopathies. Expand
Activation of CD36 inhibits and induces regression of inflammatory corneal neovascularization.
TLDR
CD36 is involved both physiologically and pharmacologically in inhibition and regression of CNV, by direct effect on endothelial cells and partly by negatively regulating VEGF expression in macrophages. Expand
...
1
2
3
4
5
...