title: Regulatory Tweak/Fn14 signaling pathway as a potent target for controlling bone loss.
abstract: Metabolic bone diseases, such as rheumatoid arthritis (RA) and osteoporosis, are characterized as imbalance between bone formation and bone resorption, leading to bone microarchitecture damage and bone mineral density loss. Bone loss is huge threat for older people's health, which imposes a heavy financial burden on patients and their families. However, the effectiveness of bone loss treatment in clinical practice is limited. With the understanding of the molecular and cellular regulators and mediators of bone remodelling, we know that some signaling pathways and inflammatory cytokines play important roles in the development of RA and osteoporosis. The increasing evidence showed that tumor necrosis factor (TNF)-like weak inducer of apoptosis (Tweak)/fibroblast growth factor-inducible 14 (Fn14) signalling controls a variety of cellular activities in biological processes, such as proliferation, differentiation, and apoptosis and has diverse biological functions in pathological mechanisms like inflammation that are associated with the process of bone metabolism. Recent studies suggest that the interactions between Tweak/Fn14 play critical roles in osteoblast and osteoclast differentiation and apoptosis, especially in those rheumatoid arthritis patients. These findings suggest that interventions targeting Tweak/Fn14 signaling pathway to regulate osteoblast-osteoclast coupling according to its biological effects, which results in promoting osteoblast formation and inhibiting osteoclast resorption, may be a promising approach for bone loss prevention and treatment in the near future.
authors.affiliation: Department of Trauma Orthopedics, Tengzhou Central People's Hospital, Shandong, PR China.
authors.forename: Yan-Ying
authors.initials: YY
authors.lastname: Du
authors.affiliation: Department of Trauma Orthopedics, Tengzhou Central People's Hospital, Shandong, PR China.
authors.forename: Yan-Xia
authors.initials: YX
authors.lastname: Zhao
authors.affiliation: Department of Trauma Orthopedics, Tengzhou Central People's Hospital, Shandong, PR China. Electronic address: liu9534@sohu.com.
authors.forename: Yu-Ping
authors.initials: YP
authors.lastname: Liu
authors.affiliation: Department of Trauma Orthopedics, Tengzhou Central People's Hospital, Shandong, PR China.
authors.forename: Wei
authors.initials: W
authors.lastname: Liu
authors.affiliation: Department of Trauma Orthopedics, Tengzhou Central People's Hospital, Shandong, PR China.
authors.forename: Ming-Ming
authors.initials: MM
authors.lastname: Wang
authors.affiliation: Department of Trauma Orthopedics, Tengzhou Central People's Hospital, Shandong, PR China.
authors.forename: Chong-Ming
authors.initials: CM
authors.lastname: Yuan
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D050071:Bone Density Conservation Agents / Q000008:administration & dosage; D016723:Bone Remodeling / Q000187:drug effects / Q000502:physiology; D000074049:Cytokine TWEAK; D006801:Humans; D010010:Osteoclasts / Q000187:drug effects / Q000378:metabolism*; D010024:Osteoporosis / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*; D000074050:TWEAK Receptor; D048069:Tumor Necrosis Factors / Q000378:metabolism*
chemical_list: D050071:Bone Density Conservation Agents; D000074049:Cytokine TWEAK; D018124:Receptors, Tumor Necrosis Factor; C000613297:TNFRSF12A protein, human; C109743:TNFSF12 protein, human; D000074050:TWEAK Receptor; D048069:Tumor Necrosis Factors
keywords: Bone loss; Tweak/fn14