title: Targeting VEGF and Its Receptors for the Treatment of Osteoarthritis and Associated Pain.
abstract: Increased vascular endothelial growth factor (VEGF) levels are associated with osteoarthritis (OA) progression. Indeed, VEGF appears to be involved in OA-specific pathologies including cartilage degeneration, osteophyte formation, subchondral bone cysts and sclerosis, synovitis, and pain. Moreover, a wide range of studies suggest that inhibition of VEGF signaling reduces OA progression. This review highlights both the potential significance of VEGF in OA pathology and pain, as well as potential benefits of inhibition of VEGF and its receptors as an OA treatment. With the emergence of the clinical use of anti-VEGF therapy outside of OA, both as high-dose systemic treatments and low-dose local treatments, these particular therapies are now more widely understood. Currently, there is no established disease-modifying drug available for patients with OA, which warrants continued study of the inhibition of VEGF signaling in OA, as stand-alone or adjuvant therapy. © 2016 American Society for Bone and Mineral Research.
authors.affiliation: Department of Biochemistry, Rush University Medical Center, Chicago, IL, USA.
authors.forename: John L
authors.initials: JL
authors.lastname: Hamilton
authors.affiliation: Department of Developmental Biology, Harvard School of Dental Medicine, Boston, MA, USA.
authors.forename: Masashi
authors.initials: M
authors.lastname: Nagao
authors.affiliation: Department of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, USA.
authors.forename: Brett R
authors.initials: BR
authors.lastname: Levine
authors.affiliation: Department of Biochemistry, Rush University Medical Center, Chicago, IL, USA.
authors.forename: Di
authors.initials: D
authors.lastname: Chen
authors.affiliation: Department of Developmental Biology, Harvard School of Dental Medicine, Boston, MA, USA.
authors.forename: Bjorn R
authors.initials: BR
authors.lastname: Olsen
authors.affiliation: Department of Biochemistry, Rush University Medical Center, Chicago, IL, USA.|Department of Orthopedic Surgery, Rush University Medical Center, Chicago, IL, USA.|Internal Medicine Section of Rheumatology, Rush University Medical Center, Chicago, IL, USA.|Department of Bioengineering, University of Illinois, Chicago, IL, USA.|Jesse Brown Veterans Affairs, Chicago, IL, USA.
authors.forename: Hee-Jeong
authors.initials: HJ
authors.lastname: Im
mesh_terms: D005260:Female; D006801:Humans; D008297:Male; D010003:Osteoarthritis / Q000188:drug therapy* / Q000378:metabolism; D010146:Pain / Q000188:drug therapy* / Q000378:metabolism; D015398:Signal Transduction; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors* / Q000378:metabolism
chemical_list: C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A
keywords: ANGIOGENESIS; OSTEOARTHRITIS; VASCULAR ENDOTHELIAL GROWTH FACTOR (VEGF); VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR (VEGFR)