NGF x RANKL

Last update 08 May 2025

Basic Info

Related Targets

NGFRANKL

Drugs associated with NGF x RANKL

Anti-RANKL/NGF antibody (Jiangsu hengrui)

Target

NGF x RANKL

Mechanism

NGF inhibitors [+1]

Active Org.

Jiangsu Hengrui Pharmaceuticals Co., Ltd.

Originator Org.

Jiangsu Hengrui Pharmaceuticals Co., Ltd.

Active Indication

Neoplasms [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with NGF x RANKL

100 Translational Medicine associated with NGF x RANKL

0 Patents (Medical) associated with NGF x RANKL

Literatures (Medical) associated with NGF x RANKL

01 Mar 2025·Journal of Orthopaedic Translation

Hyperbaric oxygen potentiates platelet-rich plasma composition and accelerates bone healing

Article

Author: Chen, Tzu-Hao ; Chang, Ching-Ping ; Chao, Ssu-Han ; Chien, Chi-Sheng ; Huang, Chien-Cheng ; Lin, Cheng-Hsien ; Chang, Wen-Shuo

ObjectiveThis study aimed to investigate whether platelet-rich plasma (PRP) obtained from the blood of rats preconditioned with hyperbaric oxygen (HBOP) would enhance the biological activity of PRP and accelerate the healing process of femur fractures in a rat model.DesignPRP was derived from blood samples of healthy rats subjected to either hyperbaric oxygen (hPRP) or normobaric air (nPRP). A closed femur fracture model was established in male Wistar rats, with treatments of hPRP or nPRP administered around the fracture site immediately post-fracture and on days 7, 14, 21, and 28. Growth factor concentrations in hPRP and nPRP were biochemically quantified. Bone healing was assessed weekly by X-ray, while histological and immunofluorescence analyses evaluated inflammatory status, osteoprotegerin (OPG), receptor activator of nuclear factor kappa-B ligand (RANKL) expression, and the presence of osteoblasts, osteoclasts, and osteocytes during healing. The effects of hPRP and nPRP on MC3T3-E1 preosteoblast migration and proliferation were also tested in vitro.ResultshPRP showed significantly higher concentrations of growth factors such as activin-A, brain-derived neurotrophic factor, nerve growth factor, Flt-3 Ligand, granulocyte-macrophage colony-stimulating factor, hepatocyte growth factor, and platelet-derived growth factor, compared to nPRP. In vitro, hPRP demonstrated more significant effects on preosteoblast migration and proliferation. In vivo, hPRP treatment resulted in enhanced bone healing, higher OPG levels in osteoblasts and osteoclasts, and an elevated OPG/RANKL ratio compared to nPRP.ConclusionsHBOP enhances the biological activity of PRP and accelerates bone healing in a closed femur fracture model in rats. This study highlights the regenerative potential of PRP when preconditioned with hyperbaric oxygen for use in bone fracture therapy.Significance statementPRP is widely used in treating bone defects and fractures, but its enhancement through HBOP remains underexplored. Our findings demonstrate that HBOP potentiates the biological activity of PRP, offering promising therapeutic potential for bone fracture healing.The translational potential of this articleEnriching growth factors in PRP through HBOP could significantly improve tissue regeneration, especially in bone healing. The potential of hPRP in clinical applications is highly promising, particularly in orthopaedic surgery, trauma care, sports medicine, and managing bone healing in compromised patients.

01 Jan 2025·Discovery Medicine

Neuro-Immuno-Endocrine Regulation of Bone Homeostasis

Review

Author: Maurya, Ranjeet ; Kharwar, Rajesh Kumar ; Singh, Vineet Kumar ; Banoriya, Gaurav Kumar

Bone is an important connective tissue involved in the movement and mechanical support of the body. Its homeostasis refers to the equilibrium between bone formation by osteoblasts and bone resorption by osteoclasts. Hematopoietic progenitor cells are shared by bone and immune cells, and the skeletal system is extensively innervated by an extensive nerve network. The immune, endocrine and nervous systems synthesize and secrete cytokines, hormones and neurotransmitters, respectively, which regulate physiological processes involved in bone homeostasis. Hormones such as gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), luteinizing hormone (LH), estrogen, testosterone, insulin, thyroxine, parathyroid hormone (PTH), calcitonin, etc., regulate bone formation and resorption. Tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β), granulocyte-macrophage colony-stimulating factor (GM-CSF), and interleukin (interleukin (IL)-1,3,4,6,10,17,18,23,27) regulate the function of osteoblasts and osteoclasts as well as the bone microenvironment. The skeleton is innervated by sympathetic, parasympathetic and sensory nerve fibers that release neurotransmitters/factors such as serotonin, nerve growth factor, neuropeptide Y, substance P, norepinephrine and acetylcholine, which interact with various cells in the bone. Sclerostin, osteopontin, osteoprotegerin, osteocalcin, prostaglandin E2 and receptor activator of nuclear factor-kappa B ligand (RANKL)/receptor activator of nuclear factor-kappa B (RANK) are some of the important proteins released by osteoblasts, osteocytes and osteoclasts that regulate osteoblastogenesis, osteoclastogenesis and angiogenesis and are also involved in pathological conditions. Further research is needed to establish links between the skeleton and other tissues and to gain additional insights into the etiology of degenerative diseases and the drug development process. The aim of this minireview is therefore to understand the composition of bone and the maintenance of bone homeostasis through three coordinates, namely the endocrine, nervous and immune systems.

01 Mar 2024·JOR SPINE

Targeted screening of inflammatory mediators in spontaneous degenerative disc disease in dogs reveals an upregulation of the tumor necrosis superfamily

Article

Author: Meij, Björn P. ; Krupkova, Olga ; Smolders, Lucas A. ; Ettinger, Ladina ; Pozzi, Antonio ; Schmid, David ; Wuertz‐Kozak, Karin ; Steffen, Frank ; Tryfonidou, Marianna A. ; Bach, Frances C. ; Bitterli, Thomas

AbstractBackgroundThe regulation of inflammatory mediators in the degenerating intervertebral disc (IVD) and corresponding ligamentum flavum (LF) is a topic of emerging interest. The study aimed to investigate the expression of a broad array of inflammatory mediators in the degenerated LF and IVD using a dog model of spontaneous degenerative disc disease (DDD) to determine potential treatment targets.MethodsLF and IVD tissues were collected from 22 normal dogs (Pfirrmann grades I and II) and 18 dogs affected by DDD (Pfirrmann grades III and IV). A qPCR gene array was used to investigate the expression of 80 inflammatory genes for LF and IVD tissues, whereafter targets of interest were investigated in additional tissue samples using qPCR, western blot (WB), and immunohistochemistry.ResultsTumor necrosis factor superfamily (TNFSF) signaling was identified as a regulated pathway in DDD, based on the significant regulation (n‐fold ± SD) of various TNFSF members in the degenerated IVD, including nerve growth factor (NGF; −8 ± 10), CD40LG (464 ± 442), CD70 (341 ± 336), TNFSF Ligand 10 (9 ± 8), and RANKL/TNFSF Ligand 11 (85 ± 74). In contrast, TNFSF genes were not significantly affected in the degenerated LF compared to the control LF. Protein expression of NGF (WB) was significantly upregulated in both the degenerated LF (4.4 ± 0.5) and IVD (11.3 ± 5.6) compared to the control group. RANKL immunopositivity was significantly upregulated in advanced stages of degeneration (Thompson grades IV and V) in the nucleus pulposus and annulus fibrosus of the IVD, but not in the LF.ConclusionsDDD involves a significant upregulation of various TNFSF members, with tissue‐specific expression profiles in LF and IVD tissues. The differential involvement of TNFSF members within multiple spinal tissues from the same individual provides new insights into the inflammatory processes involved in DDD and may provide a basis to formulate hypotheses for the determination of potential treatment targets.

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