INTRODUCTIONThe transforming growth factor-β （TGF-β） superfamily com- prises TGF-βs, Activin, bone morphogenetic proteins （BMPs） and other related proteins. TGF-β superfamily members act through a heteromeric ...INTRODUCTIONThe transforming growth factor-β （TGF-β） superfamily com- prises TGF-βs, Activin, bone morphogenetic proteins （BMPs） and other related proteins. TGF-β superfamily members act through a heteromeric receptor complex,, comprised of type I and type II receptors at the cell surface that transduce intracellular signals via Smad complex or mitogen-activated protein kinase （MAPK） cascade.展开更多
背景:正畸力通过多种信号通路激活牙周组织自噬,进一步增强或减弱相关细胞(牙周膜细胞、骨细胞、破骨细胞和成骨细胞等)的活性来促进牙周重塑。目的:综述目前正畸力介导牙周组织自噬的研究进展和其对正畸牙齿移动的影响。方法:在PubMed...背景:正畸力通过多种信号通路激活牙周组织自噬,进一步增强或减弱相关细胞(牙周膜细胞、骨细胞、破骨细胞和成骨细胞等)的活性来促进牙周重塑。目的:综述目前正畸力介导牙周组织自噬的研究进展和其对正畸牙齿移动的影响。方法:在PubMed、Web of Science、中国生物医学文献数据库和中国知网数据库进行文献检索,设置检索时限为2010-2023年,总结了2010年以来正畸与自噬相关研究进展,最终纳入76篇文献进行分析讨论。结果与结论:(1)正畸力可通过牙周机械感受器和其造成的无菌性炎症引发一系列生物化学信号的转变,进而引起牙周组织自噬。(2)自噬通过级联放大的信号通路如磷脂酰肌醇-3-激酶/蛋白激酶B通路、河马通路及丝裂原活化蛋白激酶通路等,产生相应反馈从而促进牙周组织改建,最终实现牙齿的移动与稳定。正畸力诱导的自噬可差异性调节牙齿压力侧骨吸收和张力侧骨形成,相关靶点在正畸临床治疗的应用中具有良好前景。(3)然而,正畸力与自噬的机制较为复杂,现有研究仅停留在探究自噬对正畸牙齿移动的作用,自噬与正畸牙齿移动过程中的相互调节作用、涉及相关通路上游机械受体及信号通路间的交互作用均需要进一步的探究。展开更多
Integrin-mediated adhesions play critical roles in diverse cell functions. Integrins offers a platform on which mechanical stimuli, cytoskeletal organization, biochemical signals can concentrate. Mechanical stimuli tr...Integrin-mediated adhesions play critical roles in diverse cell functions. Integrins offers a platform on which mechanical stimuli, cytoskeletal organization, biochemical signals can concentrate. Mechanical stimuli transmitted by integrins influence the cytoskeleton, in turn, the cytoskeleton influences cell adhesion via integrins, then cell adhesion results in a series of signal transduction cascades. In skeleton, integrins also have a key role for bone resoption by osteoclasts and reformation by osteoblasts. In present review, the proteins involved in integrin signal transduction and integrin signal transduction pathways were discussed, mainly on the basic mechanisms of integrin signaling and the roles of integrins in bone signal transduction, which may give insight into new therapeutic agents to all kinds of skeletal diseases and new strategies for bone tissue engineering.展开更多
基金supported by grants by NIH grant AR-044741(Y-PL) and R01DE023813 (Y-PL)
文摘INTRODUCTIONThe transforming growth factor-β （TGF-β） superfamily com- prises TGF-βs, Activin, bone morphogenetic proteins （BMPs） and other related proteins. TGF-β superfamily members act through a heteromeric receptor complex,, comprised of type I and type II receptors at the cell surface that transduce intracellular signals via Smad complex or mitogen-activated protein kinase （MAPK） cascade.
文摘背景:正畸力通过多种信号通路激活牙周组织自噬,进一步增强或减弱相关细胞(牙周膜细胞、骨细胞、破骨细胞和成骨细胞等)的活性来促进牙周重塑。目的:综述目前正畸力介导牙周组织自噬的研究进展和其对正畸牙齿移动的影响。方法:在PubMed、Web of Science、中国生物医学文献数据库和中国知网数据库进行文献检索,设置检索时限为2010-2023年,总结了2010年以来正畸与自噬相关研究进展,最终纳入76篇文献进行分析讨论。结果与结论:(1)正畸力可通过牙周机械感受器和其造成的无菌性炎症引发一系列生物化学信号的转变,进而引起牙周组织自噬。(2)自噬通过级联放大的信号通路如磷脂酰肌醇-3-激酶/蛋白激酶B通路、河马通路及丝裂原活化蛋白激酶通路等,产生相应反馈从而促进牙周组织改建,最终实现牙齿的移动与稳定。正畸力诱导的自噬可差异性调节牙齿压力侧骨吸收和张力侧骨形成,相关靶点在正畸临床治疗的应用中具有良好前景。(3)然而,正畸力与自噬的机制较为复杂,现有研究仅停留在探究自噬对正畸牙齿移动的作用,自噬与正畸牙齿移动过程中的相互调节作用、涉及相关通路上游机械受体及信号通路间的交互作用均需要进一步的探究。
文摘Integrin-mediated adhesions play critical roles in diverse cell functions. Integrins offers a platform on which mechanical stimuli, cytoskeletal organization, biochemical signals can concentrate. Mechanical stimuli transmitted by integrins influence the cytoskeleton, in turn, the cytoskeleton influences cell adhesion via integrins, then cell adhesion results in a series of signal transduction cascades. In skeleton, integrins also have a key role for bone resoption by osteoclasts and reformation by osteoblasts. In present review, the proteins involved in integrin signal transduction and integrin signal transduction pathways were discussed, mainly on the basic mechanisms of integrin signaling and the roles of integrins in bone signal transduction, which may give insight into new therapeutic agents to all kinds of skeletal diseases and new strategies for bone tissue engineering.
