Key Triggers of Osteoclast-Related Diseases and Available Strategies for Targeted Therapies: A Review.
Key Triggers of Osteoclast-Related Diseases and Available Strategies for Targeted Therapies: A Review.
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破骨细胞相关疾病的关键触发因素和可用的靶向治疗策略:综述
DOI:
10.3389/fmed.2017.00234
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发表时间:
2017
影响因子:
3.9
通讯作者:
Dai M
中科院分区:
文献类型:
--
作者:
Bi H;Chen X;Gao S;Yu X;Xiao J;Zhang B;Liu X;Dai M
Osteoclasts, the only cells with bone resorption functions in vivo, maintain the balance of bone metabolism by cooperating with osteoblasts, which are responsible for bone formation. Excessive activity of osteoclasts causes many diseases such as osteoporosis, periprosthetic osteolysis, bone tumors, and Paget’s disease. In contrast, osteopetrosis results from osteoclast deficiency. Available strategies for combating over-activated osteoclasts and the subsequently induced diseases can be categorized into three approaches: facilitating osteoclast apoptosis, inhibiting osteoclastogenesis, and impairing bone resorption. Bisphosphonates are representative molecules that function by triggering osteoclast apoptosis. New drugs, such as tumor necrosis factor and receptor activator of nuclear factor kappa-B ligand (RANKL) inhibitors (e.g., denosumab) have been developed for targeting the receptor activator of nuclear factor kappa-B /RANKL/osteoprotegerin system or CSF-1/CSF-1R axis, which play critical roles in osteoclast formation. Furthermore, vacuolar (H+)-ATPase inhibitors, cathepsin K inhibitors, and glucagon-like peptide 2 impair different stages of the bone resorption process. Recently, significant achievements have been made in this field. The aim of this review is to provide an updated summary of the current progress in research involving osteoclast-related diseases and of the development of targeted inhibitors of osteoclast formation.
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影响因子:
3.7
作者:
Chen ZF;Matsumura K;Wang H;Arellano SM;Yan X;Alam I;Archer JA;Bajic VB;Qian PY
通讯作者:
Qian PY
影响因子:
4.9
作者:
Garcia S;Hartkamp LM;Malvar-Fernandez B;van Es IE;Lin H;Wong J;Long L;Zanghi JA;Rankin AL;Masteller EL;Wong BR;Radstake TR;Tak PP;Reedquist KA
通讯作者:
Reedquist KA
影响因子:
6.2
作者:
Chen, Gaoping;Sircar, Kanishka;Rabbani, Shafaat A.
通讯作者:
Rabbani, Shafaat A.
影响因子:
15.9
作者:
Cenci, S;Weitzmann, MN;Pacifici, R
通讯作者:
Pacifici, R
影响因子:
44.5
作者:
Bone, Henry G.;Wagman, Rachel B.;Papapoulos, Socrates
通讯作者:
Papapoulos, Socrates