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1 pression of VEGFA and were protected against pathological neovascularization.
2 quired for normal vessel development and for pathological neovascularization.
3 he retina, suggesting that PGC-1alpha drives pathological neovascularization.
4 uld emerge as a good target for treatment of pathological neovascularization.
5 a useful therapeutic approach in diseases of pathological neovascularization.
6 already-established target for treatment of pathological neovascularization.
7 ed vascular loss followed by hypoxia-induced pathological neovascularization.
8 not protect the retina, but rather enhanced pathological neovascularization.
9 of many devastating diseases with associated pathological neovascularization.
10 st retinal vessels while suppressing ectopic pathological neovascularization.
11 terized by invasive synovial hyperplasia and pathological neovascularization.
12 have been shown to contribute to normal and pathological neovascularization.
13 etinal ischemia can cause vision-threatening pathological neovascularization.
14 novel target for the design of inhibitors of pathological neovascularization.
15 odronate-liposomes led to the suppression of pathological neovascularization.
16 ponses with an anti-CD2 antibody exacerbated pathological neovascularization.
17 etina, leads to signals for compensatory but pathological neovascularization.
18 SPP1 resulted in a significant reduction in pathological neovascularization.
19 omotes alternative macrophage activation and pathological neovascularization.
20 in RNA targeting Sema3e promoted disoriented pathological neovascularization and partially abolished
21 chemical inhibitor substantially reduced the pathological neovascularization and rescued visual funct
22 del to test the role of nitric oxide (NO) in pathological neovascularization and vessel permeability.
23 morphonuclear leukocytes (PMN) infiltration, pathological neovascularization, and up-regulation of me
24 t paper, the mechanisms of physiological and pathological neovascularization are compared and contras
25 ctors (VEGFs) are mainly responsible for the pathological neovascularization as in the case in neovas
27 expression of ADAM9 could potentially affect pathological neovascularization by increasing the sheddi
28 e findings may lead to methods of regulating pathological neovascularization by specifically targetin
29 eutic use, especially in retinopathies where pathological neovascularization compromises vision and l
30 fining the molecular pathways distinguishing pathological neovascularization from normal vessels is c
31 he role of this endogenous LXA(4) circuit in pathological neovascularization has not been determined.
32 and activity are significantly increased in pathological neovascularization in a mouse model of oxyg
33 r regrowth after injury, and hypoxia-induced pathological neovascularization in a mouse model of oxyg
34 VEGF) is the angiogenic factor promoting the pathological neovascularization in age-related macular d
36 TNF-alpha blockade diminished the enhanced pathological neovascularization in APN-KO mice by 34%, a
40 retinal vascular development and suppresses pathological neovascularization in oxygen-induced retino
41 c MPs were selectively recruited to sites of pathological neovascularization in response to locally p
42 elial growth factor (VEGF) treatments reduce pathological neovascularization in the eye and in tumors
44 demonstrate that TIMP3 and erlotinib inhibit pathological neovascularization in the mouse retina, mos
50 ch3 is induced in hypoxia and interestingly, pathological neovascularization is decreased in retinas
51 elium and limbus in corneal avascularity and pathological neovascularization (NV) is not well underst
54 P), loss of Casp-8 in ECs was beneficial, as pathological neovascularization was reduced in Casp-8ECK
55 tently suppressed the leukocyte adhesion and pathological neovascularization, whereas it had little o
56 us contribute to postnatal physiological and pathological neovascularization, which is consistent wit
58 hibitors as therapeutic agents in inhibiting pathological neovascularization with a range of clinical
59 pecific deletion of Angptl4 showed decreased pathological neovascularization with stable vessel struc
60 inhibitors of angiogenesis are able to block pathological neovascularization without harming the pree