scholarly journals Insulin-like growth factor-1 in articular cartilage repair for osteoarthritis treatment

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Caining Wen ◽  
Limei Xu ◽  
Xiao Xu ◽  
Daping Wang ◽  
Yujie Liang ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Growth Factor ◽  
Cartilage Repair ◽  
Critical Issue ◽  
Delivery Systems ◽  
Chondrocyte Apoptosis ◽  
Insulin Like Growth Factor ◽  
Articular Cartilage Repair ◽  
Osteoarthritis Treatment

AbstractArticular cartilage repair is a critical issue in osteoarthritis (OA) treatment. The insulin-like growth factor (IGF) signaling pathway has been implicated in articular cartilage repair. IGF-1 is a member of a family of growth factors that are structurally closely related to pro-insulin and can promote chondrocyte proliferation, enhance matrix production, and inhibit chondrocyte apoptosis. Here, we reviewed the role of IGF-1 in cartilage anabolism and catabolism. Moreover, we discussed the potential role of IGF-1 in OA treatment. Of note, we summarized the recent progress on IGF delivery systems. Optimization of IGF delivery systems will facilitate treatment application in cartilage repair and improve OA treatment efficacy.

Articular Cartilage Repair with Autografting Under the Influence of Insulin-Like Growth Factor-1 in Rabbits

2007 ◽  
Vol 54 (4) ◽  
pp. 210-218 ◽  
Author(s):  
N. K. Singh ◽  
G. R. Singh ◽  
P. Kinjavdekar ◽  
A. K. Sharma ◽  
T. R. Mohanty ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Growth Factor ◽  
Cartilage Repair ◽  
Insulin Like Growth Factor ◽  
Articular Cartilage Repair

Articular cartilage repair by gene therapy using growth factor-producing mesenchymal cells

2003 ◽  
Vol 48 (2) ◽  
pp. 430-441 ◽  
Author(s):  
Kolja Gelse ◽  
Klaus von der Mark ◽  
Thomas Aigner ◽  
Jung Park ◽  
Holm Schneider
Keyword(s):  
Gene Therapy ◽  
Articular Cartilage ◽  
Growth Factor ◽  
Cartilage Repair ◽  
Mesenchymal Cells ◽  
Articular Cartilage Repair

scholarly journals The Contributive Role of IGFBP-3 and Mitochondria in Synoviocyte-Induced Osteoarthritis through Hypoxia/Reoxygenation Injury: A Pathogenesis-Focused Literature Review

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Daniel Gululi ◽  
Guy-Armel Bounda ◽  
Jianping Li ◽  
Haohuan Li
Keyword(s):  
Growth Factor ◽  
Essential Role ◽  
Cartilage Degradation ◽  
Chondrocyte Apoptosis ◽  
Insulin Like Growth Factor ◽  
Synovial Joint ◽  
Hypoxia Inducible Factors ◽  
Igfbp 3 ◽  
Hypoxia Reoxygenation

Osteoarthritis (OA), one of the most common joint disorders, is characterized by chronic progressive cartilage degradation, osteophyte formation, and synovial inflammation. OA lesions are not only located in articular cartilage but also in the entire synovial joint. Nevertheless, most of the early studies done mostly focused on the important role of chondrocyte apoptosis and cartilage degeneration in the pathogenesis and progress of OA. The increased expression of hypoxia-inducible factors (HIF-1α and HIF-2α) is known to be the cellular and biochemical signal that mediates the response of chondrocytes to hypoxia. The role of the synovium in OA pathogenesis had been poorly evaluated. Being sensitive to hypoxia/reoxygeneration (H/R) injury, fibroblast-like synoviocytes (FLS) play an essential role in cartilage degradation during the course of this pathology. Insulin-like growth factor binding protein 3 (IGFBP-3) acts as the main carrier of insulin-like growth factor I (IGF-I) in the circulation and remains the most abundant among the six IGFBPs. Synovial fluids of OA patients have markedly increased levels of IGFBP-3. We aim to discuss the interconnected behavior of IGFBP-3 and synoviocytes during the course of osteoarthritis pathogenesis, especially under the influence of hypoxia-inducible factors. In this review, we present information related to the essential role that is played by IGFBP-3 and mitochondria in synoviocyte-induced osteoarthritis through H/R injury. Little research has been done in this area. However, strong evidences show that the level of IGFBP-3 in synovial fluid significantly increased in OA, inhibiting the binding of IGF-1 to IGFR 1 (IGF receptor-1) and therefore the inhibition of cell proliferation. To the best of our knowledge, this is the first paper providing a comprehensive explanatory contribution of IGFBP-3 and mitochondria in synovial cell-induced osteoarthritis through hypoxia/reoxygenation mechanism.

scholarly journals Hydrogel-Based Controlled Delivery Systems for Articular Cartilage Repair

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Ana Rey-Rico ◽  
Henning Madry ◽  
Magali Cucchiarini
Keyword(s):  
Articular Cartilage ◽  
Cartilage Repair ◽  
Inflammatory Responses ◽  
Delivery Systems ◽  
Controlled Delivery ◽  
Bioactive Molecules ◽  
Therapeutic Action ◽  
Articular Cartilage Repair ◽  
Spatial Presentation ◽  
Temporal And Spatial

Delivery of bioactive factors is a very valuable strategy for articular cartilage repair. Nevertheless, the direct supply of such biomolecules is limited by several factors including rapid degradation, the need for supraphysiological doses, the occurrence of immune and inflammatory responses, and the possibility of dissemination to nontarget sites that may impair their therapeutic action and raise undesired effects. The use of controlled delivery systems has the potential of overcoming these hurdles by promoting the temporal and spatial presentation of such factors in a defined target. Hydrogels are promising materials to develop delivery systems for cartilage repair as they can be easily loaded with bioactive molecules controlling their release only where required. This review exposes the most recent technologies on the design of hydrogels as controlled delivery platforms of bioactive molecules for cartilage repair.

scholarly journals Articular cartilage repair: the role of bone morphogenetic proteins

2002 ◽  
Vol 26 (3) ◽  
pp. 131-136 ◽  
Author(s):  
Pecina M. ◽  
Jelic M. ◽  
Martinovic S. ◽  
Haspl M. ◽  
Vukicevic S.
Keyword(s):  
Articular Cartilage ◽  
Cartilage Repair ◽  
Bone Morphogenetic Proteins ◽  
Articular Cartilage Repair
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