PMID- 23329331
OWN - NLM
STAT- MEDLINE
DCOM- 20130903
LR  - 20220408
IS  - 1432-1440 (Electronic)
IS  - 0946-2716 (Print)
IS  - 0946-2716 (Linking)
VI  - 91
IP  - 3
DP  - 2013 Mar
TI  - Ocular neovascularization.
PG  - 311-21
LID - 10.1007/s00109-013-0993-5 [doi]
AB  - Retinal and choroidal vascular diseases constitute the most common causes of 
      moderate and severe vision loss in developed countries. They can be divided into 
      retinal vascular diseases, in which there is leakage and/or neovascularization 
      (NV) from retinal vessels, and subretinal NV, in which new vessels grow into the 
      normally avascular outer retina and subretinal space. The first category of 
      diseases includes diabetic retinopathy, retinal vein occlusions, and retinopathy 
      of prematurity, and the second category includes neovascular age-related macular 
      degeneration (AMD), ocular histoplasmosis, pathologic myopia, and other related 
      diseases. Retinal hypoxia is a key feature of the first category of diseases 
      resulting in elevated levels of hypoxia-inducible factor-1 (HIF-1) which 
      stimulates expression of vascular endothelial growth factor (VEGF), 
      platelet-derived growth factor-B (PDGF-B), placental growth factor, 
      stromal-derived growth factor-1 and their receptors, as well as other 
      hypoxia-regulated gene products such as angiopoietin-2. Although hypoxia has not 
      been demonstrated as part of the second category of diseases, HIF-1 is elevated 
      and thus the same group of hypoxia-regulated gene products plays a role. Clinical 
      trials have shown that VEGF antagonists provide major benefits for patients with 
      subretinal NV due to AMD and even greater benefits are seen by combining 
      antagonists of VEGF and PDGF-B. It is likely that addition of antagonists of 
      other agents listed above will be tested in the future. Other appealing 
      strategies are to directly target HIF-1 or to use gene transfer to express 
      endogenous or engineered anti-angiogenic proteins. While substantial progress has 
      been made, the future looks even brighter for patients with retinal and choroidal 
      vascular diseases.
FAU - Campochiaro, Peter A
AU  - Campochiaro PA
AD  - Departments of Ophthalmology and Neuroscience, Johns Hopkins University School of 
      Medicine, Baltimore, MD 21287-9277, USA. pcampo@jhmi.edu
LA  - eng
GR  - R01 EY012609/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20130118
PL  - Germany
TA  - J Mol Med (Berl)
JT  - Journal of molecular medicine (Berlin, Germany)
JID - 9504370
RN  - 0 (Angiopoietin-2)
RN  - 0 (HIF1A protein, human)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (Proto-Oncogene Proteins c-sis)
RN  - 0 (VEGFA protein, human)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 1B56C968OA (Becaplermin)
SB  - IM
MH  - Angiopoietin-2/metabolism
MH  - Becaplermin
MH  - *Choroidal Neovascularization/metabolism/physiopathology
MH  - Clinical Trials as Topic
MH  - Eye/*metabolism/physiopathology
MH  - Humans
MH  - Hypoxia-Inducible Factor 1, alpha Subunit/metabolism
MH  - *Macular Degeneration/metabolism/physiopathology
MH  - Proto-Oncogene Proteins c-sis/metabolism
MH  - *Retinal Neovascularization/metabolism/physiopathology
MH  - Retinal Vessels/*metabolism/physiopathology
MH  - Vascular Endothelial Growth Factor A/metabolism
PMC - PMC3584193
MID - NIHMS437116
EDAT- 2013/01/19 06:00
MHDA- 2013/09/04 06:00
PMCR- 2014/03/01
CRDT- 2013/01/19 06:00
PHST- 2012/12/20 00:00 [received]
PHST- 2013/01/02 00:00 [accepted]
PHST- 2012/12/22 00:00 [revised]
PHST- 2013/01/19 06:00 [entrez]
PHST- 2013/01/19 06:00 [pubmed]
PHST- 2013/09/04 06:00 [medline]
PHST- 2014/03/01 00:00 [pmc-release]
AID - 10.1007/s00109-013-0993-5 [doi]
PST - ppublish
SO  - J Mol Med (Berl). 2013 Mar;91(3):311-21. doi: 10.1007/s00109-013-0993-5. Epub 
      2013 Jan 18.