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| 1 | Wnt/β-catenin signalling:function,biological mechanisms,and therapeutic opportunities显示文摘The Wnt/β-catenin pathway comprises a family of proteins that play critical roles in embryonic development and adult tissue homeostasis.The deregulation of Wnt/β-catenin signalling often leads to various serious diseases,including cancer and non-cancer diseases.Although many articles have reviewed Wnt/β-catenin from various aspects,a systematic review encompassing the origin,composition,function,and clinical trials of the Wnt/β-catenin signalling pathway in tumour and diseases is lacking.In this article,we comprehensively review the Wnt/β-catenin pathway from the above five aspects in combination with the latest research.Finally,we propose challenges and opportunities for the development of small-molecular compounds targeting the Wnt signalling pathway in disease treatment. | Jiaqi Liu Qing Xiao Jiani Xiao Chenxi Niu Yuanyuan Li Xiaojun Zhang Zhengwei Zhou Guang Shu Gang Yin | 2022 | Signal Transduction and Targeted Therapy2022，7，2： | 28 |
| 2 | Copy number alteration profiling facilitates differential diagnosis between ossifying fibroma and fibrous dysplasia of the jaws显示文摘Ossifying fibroma(OF)and fibrous dysplasia(FD)are two fibro-osseous lesions with overlapping clinicopathological features,making diagnosis challenging.In this study,we applied a whole-genome shallow sequencing approach to facilitate differential diagnosis via precise profiling of copy number alterations(CNAs)using minute amounts of DNA extracted from morphologically correlated microdissected tissue samples.Freshly frozen tissue specimens from OF(n=29)and FD(n=28)patients were obtained for analysis.Lesion fibrous tissues and surrounding normal tissues were obtained by laser capture microdissection(LCM),with~30–50 cells(5000–10000µm2)per sample.We found that the rate of recurrent CNAs in OF cases was much higher(44.8%,13 of 29)than that in FD cases(3.6%,1 of 28).Sixty-nine percent(9 of 13)of the CNA-containing OF cases involved segmental amplifications and deletions on Chrs 7 and 12.We also identified eight CNA-associated genes(HILPDA,CALD1,C1GALT1,MICALL2,PHF14,AIMP2,MDM2,and CDK4)with amplified expression,which was consistent with the copy number changes.We further confirmed a jaw lesion with a previous uncertain diagnosis due to its ambiguous morphological features and the absence of GNAS mutation as OF based on the typical Chr 12 amplification pattern in its CNA profile.Moreover,analysis of a set of longitudinal samples collected from an individual with a cellular lesion in suspicion of OF at the first surgery,recurrence and the latest malignant transformation revealed identical CNA patterns at the three time points,suggesting that copy number profiling can be used as an important tool to identify borderline lesions or lesions with malignant potential.Overall,CNA profiling of fibro-osseous lesions can greatly improve differential diagnosis between OF and FD and help predict disease progression. | Ming Ma Lu Liu Ruirui Shi Jianyun Zhang Xiaotian Li Xuefen Li Jiaying Bai Jianbin Wang Yanyi Huang Tiejun Li | 2021 | International Journal of Oral Science2021，13，2： | 3 |
| 3 | Disturbed bone remodelling activity varies in different stages of experimental, gradually progressive apical periodontitis in rats显示文摘Bone remodelling keeps going through the lifespan of human by bone formation and bone resorption.In the craniofacial region,mandibles act as the main force for biting and chewing,and also become susceptible to a common bone-loss disease,namely,apical periodontitis,once infected dental pulp is not treated timely,during which bone resorption occurs from the apical foramen to the apical bone area.Although conventional root canal treatment(RCT)can remove the most of the infection,chronical apical periodontitis due to incomplete removal of dental pulp and subsequent microleakage will become refractory and more challenging,and this process has scarcely been specifically studied as a bone remodelling issue in rat models.Therefore,to study chronical and refractory apical periodontitis owing to incomplete cleaning of infected dental pulp and microleackage in vivo,we establish a modified rat model of gradually progressive apical periodontitis by sealing residual necrotic dental pulp and introducing limited saliva,which simulates gradually progressive apical periodontitis,as observed in the clinical treatment of chronical and refractory apical periodontitis.We show that bone-loss is inevitable and progressive in this case of apical periodontitis,which confirms again that complete and sound root canal treatment is crucial to halt the progression of chronical and refractory apical periodontitis and promote bone formation.Interestingly,bone remodelling was enhanced at the initial stage of apical periodontitis in this model while reduced with a high osteoblast number afterwards,as shown by the time course study of the modified model.Suggesting that the pathological apical microenvironment reserve its hard tissue formation ability to some degree but in a disturbed manner.Hopefully,our findings can provide insights for future bone regenerative treatment for apical periodontitisassociated bone loss. | Ruoshi Xu Daimo Guo Xuedong Zhou Jianxun Sun Yachuan Zhou Yi Fan Xin Zhou Mian Wan Wei Du Liwei Zheng | 2019 | International Journal of Oral Science2019，11，4： | 1 |
| 4 | 鼠在组织工程骨促骨形成研究中的应用及进展显示文摘组织工程骨修复骨缺损作为一种现代化的优良方式,一度成为研究热点。鼠类因其经济、效果稳定、能模拟多种人类疾病模型而成为多数研究骨组织再生实验对象。本文广泛查阅近年来在鼠体内构建骨再生模型的有关文献,对将鼠应用于组织工程骨促骨形成实验中的影响因素进行综述,包括鼠的种类、性别、年龄、免疫功能、组织工程骨的移植方式以及骨缺损部位等,总结特点,以供实验者参考。 | 吴佳 刘志辉 | 2020 | 口腔医学研究2020，36，1： | 0 |
| 5 | 血钙促进生长板软骨细胞增殖的作用机理显示文摘脊椎动物生长发育需要足够外源Ca2+供给,而生长板软骨细胞在Ca2+代谢过程中发挥着重要作用。为了探究小鼠生长板软骨细胞IGF1R在Ca2+调节PTHrP/PTH1R信号传导途径中的作用机制,本研究通过Cre重组酶(Ad-Cre)的体外腺病毒感染,构建Igf1r诱导型基因敲除小鼠原代软骨细胞,借助Western blotting检测不同浓度Ca2+处理后关键蛋白因子PTHrP/PTH1R的表达情况。结果表明:高Ca2+能明显加快mGPC分化进程;Ca2+信号通过独立于IGF1R的信号传导来抑制PTH1R表达,并通过IGF1R依赖性途径抑制PTHrP表达,实现对生长板软骨细胞成熟分化的调节。小鼠生长板软骨细胞的分化速率取决于PTHrP/PTH1R与细胞外Ca2+信号传导之间相互作用的平衡状态。 | 石法亮 李龙云 程勇杰 | 2019 | 基因组学与应用生物学2019，38，10： | 0 |
| 6 | 氟骨损害相关信号通路及其交互调控作用显示文摘慢性氟中毒是一种慢性全身疾病,骨相损害主要表现为氟骨症和氟牙症。氟或氟化物通过对信号通路的多个阶段产生影响,打破骨转换动态平衡,诱导成骨/破骨细胞的分化和凋亡。本综述重点介绍了五条途径:刺猬信号、Wnt/β-连环蛋白、Notch、核因子-κB受体激活子/核因子κB受体活化因子配体/骨保护素、甲状旁腺激素通路,以及这些信号通路网络中起关键作用的连接点,发现氟能够干预信号通路中的分子活性,对骨转换进行调控,并且通路之间相互协同或拮抗,维持氟中毒环境下的骨形成和骨破坏。 | 刘纯 周星宇 杨世榕 李仲伟 贾莹 | 2021 | 环境与职业医学2021，38，7： | 0 |
| 7 | On the horizon:Hedgehog signaling to heal broken bones显示文摘Uncovering the molecular pathways that drive skeletal repair has been an ongoing challenge. Initial efforts have relied on in vitro assays to identify the key signaling pathways that drive cartilage and bone differentiation. While these assays can provide some clues, assessing specific pathways in animal models is critical. Furthermore, definitive proof that a pathway is required for skeletal repair is best provided using genetic tests. Stimulating the Hh(Hedgehog) pathway can promote cartilage and bone differentiation in cell culture assays. In addition, the application of HH protein or various pathway agonists in vivo has a positive influence on bone healing. Until recently, however, genetic proof that the Hh pathway is involved in bone repair has been lacking. Here, we consider both in vitro and in vivo studies that examine the role of Hh in repair and discuss some of the challenges inherent in their interpretation. We also identify needed areas of study considering a new appreciation for the role of cartilage during repair, the variety of cell types that may have differing roles in repair, and the recent availability of powerful lineage tracing techniques. We are optimistic that emerging genetic tools will make it possible to precisely define when and in which cells promoting Hh signaling can best promote skeletal repair, and thus, the clinical potential for targeting the Hh pathway can be realized. | Stephanie T.Kuwahara Shuwan Liu Andrew Chareunsouk Maxwell Serowoky Francesca V.Mariani | 2022 | Bone Research2022，10，1： | 0 |
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