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Hippo-YAP/TAZ signaling in breast cancer:Reciprocal regulation of microRNAs and implications in precision medicine

Genes & Diseases 2024年第2期11卷 760-771页

作者： Farzad Sadri Seyede fatemeh Hosseini Zohreh Rezaei Mohammad Fereidouni Student Research Committee Birjand University of Medical SciencesBirjand ***Iran Tabas School of Nursing Birjand University of Medical SciencesBirjand ***Iran Department of Biology University of Sistan and BaluchestanZahedan ***Iran Cellular and Molecular Research Center Birjand University of Medical SciencesBirjand ***Iran

Breast cancer is a molecularly heterogeneous disease and the most common female malignancy.In recent years,therapy approaches have evolved to accommodate molecular diversity,with a focus on more biologically based therapies to minimize negative consequences.To regulate cell fate in human breast cells,the Hippo signaling pathway has been associated with the alpha subtype of estrogen receptors.This pathway regulates tissue size,regeneration,and healing,as well as the survival of tissue-specific stem cells,proliferation,and apoptosis in a variety of organs,allowing for cell differentiation.Hippo signaling is mediated by the kinases MST1,MST2,LATS1,and LATS2,as well as the adaptor proteins SAV1 and MOB.These kinases phosphorylate the downstream effectors of the Hippo pathway,yes-associated protein(YAP),and transcriptional coactivator with PDZ-binding motif(TAZ),suppressing the expression of their downstream target genes.The Hippo signaling pathway kinase cascade plays a significant role in all cancers.Understanding the principles of this kinase cascade would prevent the occurrence of breast cancer.In recent years,small noncoding RNAs,or microRNAs,have been implicated in the development of several malignancies,including breast cancer.The interconnections between miRNAs and Hippo signaling pathway core proteins in the breast,on the other hand,remain poorly understood.In this review,we focused on highlighting the Hippo signaling system,its key parts,its importance in breast cancer,and its regulation by miRNAs and other related pathways.

关键词： Breast cancer Hippo signaling Large tumor suppressor kinase 1 microRNAs PDZ-binding motif yes-associated protein

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GRK2 mediated degradation of SAV1 initiates hyperplasia of fibroblast-like synoviocytes in rheumatoid arthritis

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Acta Pharmaceutica Sinica B 2024年第3期14卷 1222-1240页

作者： Paipai Guo Ji Jiang Rui Chu Feng He Mingli Ge Ruhong Fang Qiuyun Guan Huijuan Cheng Chunru Jiang Tiantian Su Zhenduo Zhu Hao Liu Wei Wei Shihao Zhang Qingtong Wang Institute of Clinical Pharmacology Anhui Medical UniversityKey Laboratory of Anti-inflammatory and Immune MedicineMinistry of EducationCollaborative Innovation Center of Anti-inflammatory and Immune MedicinesHefei 230032China School of Pharmacy Bengbu Medical CollegeBengbu 233030China The Third Affiliated Hospital of Anhui Medical University(the First People’s Hospital of Hefei) Hefei 230061China

Hyperplasia and migration of fibroblast-like synoviocytes(FLSs)are the key drivers in the pathogenesis of rheumatoid arthritis(RA)and joint destruction.Abundant yes-associated protein(YAP),which is a powerful transcription co-activator for proliferative genes,was observed in the nucleus of inflammatory FLSs with unknown upstream mechanisms.Using Gene Expression Omnibus database analysis,it was found that Salvador homolog-1(SAV1),the pivotal negative regulator of the Hippo-YAP pathway,was slightly downregulated in RA synovium.However,SAV1 protein expression is extremely reduced.Subsequently,it was revealed that SAV1 is phosphorylated,ubiquitinated,and degraded by interacting with an important serine-threonine kinase,G protein-coupled receptor(GPCR)kinase 2(GRK2),which was predominately upregulated by GPCR activation induced by ligands such as prostaglandin E2(PGE2)in RA.This process further contributes to the decreased phosphorylation,nuclear translocation,and transcriptional potency of YAP,and leads to aberrant FLSs proliferation.Genetic depletion of GRK2 or inhibition of GRK2 by paroxetine rescued SAV1 expression and restored YAP phosphorylation and finally inhibited RA FLSs proliferation and migration.Similarly,paroxetine treatment effectively reduced the abnormal proliferation of FLSs in a rat model of collagen-induced arthritis which was accompanied by a significant improvement in clinical manifestations.Collectively,these results elucidate the significance of GRK2 regulation of Hippo-YAP signaling in FLSs proliferation and migration and the potential application of GRK2 inhibition in the treatment of FLSs-driven joint destruction in RA.

关键词： Rheumatoid arthritis Fibroblast-like synoviocytes G protein-coupled receptor kinase 2 Salvador homolog-1 yes-associated protein

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Pien Tze Huang Inhibits Migration and Invasion of Hepatocellular Carcinoma Cells by Repressing PDGFRB/YAP/CCN2 Axis Activity

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Chinese Journal of Integrative Medicine 2024年第2期30卷 115-124页

作者： LUO Zhi-yi TIAN Qi CHENG Niang-mei LIU Wen-han YANG Ye CHEN Wei ZHANG Xiang-zhi ZHENG Xiao-yuan CHEN Ming-sheng ZHUANG Qiu-yu ZHAO Bi-xing LIU Cong-sheng LIU Xiao-long LI Qin WANG Ying-chao The United Innovation of Mengchao Hepatobiliary Technology Key Laboratory of Fujian Province Mengchao Hepatobiliary Hospital of Fujian Medical UniversityFuzhou(350025)China Fujian Pien Tze Huang Enterprise Key Laboratory of Natural Medicine Research and Development Zhangzhou Pien Tze Huang Pharmaceutical Co.Ltd.ZhangzhouFujian Province(363099)China College of Biological Science and Engineering and Mengchao Med-X Center Fuzhou UniversityFuzhou(350116)China Department of Internal Medicine Mengchao Hepatobiliary Hospital of Fujian Medical UniversityFuzhou(350025)China

Objective:To investigate the effects of Pien Tze Huang(PZH) on the migration and invasion of HCC cells and underlying molecular mechanism.Methods:Cell counting kit-8(CCK-8) was applied to evaluate the cell viabilities of SMMC-7721,SK-Hep-1,C3A and HL-7702(6 × 10^(3)cells/well) co-incubated with different concentrations of PZH(0,0.2,0.4,0.6,0.8 mg/mL) for 24 h.Transwell,wound healing assay,CCK-8and Annexin V-FITC/PI staining were conducted to investigate the effects of PZH on the migration,invasion,proliferation and apoptosis of SK-Hep-1 and SMMC-7721 cells(650 μg/mL for SK-Hep-1 cells and 330 μg/mL for SMMC-7721 cells),respectively.In vivo,lung metastasis mouse model constructed by tail vein injection of HCC cells was used for evaluating the anti-metastasis function of PZH.SK-Hep-1 cells(10^(6)cells/200 μL per mice) were injected into B-NDG mice via tail vein.Totally 8 mice were randomly divided into PZH and control groups,4 mice in each group.After 2-d inoculation,mice in the PZH group were administered with PZH(250 mg/kg,daily) and mice in the control group received only vehicle(PBS) from the 2nd day after xenograft to day 17.Transcriptome analysis based on RNA-seq was subsequently used for deciphering anti-tumor mechanism of PZH.Quantitative real-time polymerase chain reaction(qRT-PCR) and Western blot were applied to verify RNA-seq results.Luciferase reporter assay was performed to examine the transcriptional activity of yes-associated protein(YAP).Results:PZH treatment significantly inhibited the migration,invasion,proliferation and promoted the apoptosis of HCC cells in vitro and in vivo(Passociated with anti-metastasis function of PZH.Mechanical study showed PZH significantly inhibited the expressions of platelet derived growth factor receptor beta(PDGFRB),YAP,connective tissue growth factor(CCN2),N-cadherin,vimentin and matrix metallopeptidase 2(MMP2,P<0.01).Meanwhile,the phosphorylation of YAP was also enhanced by PZH treatment in v

关键词： PienTzeHuang hepatocellular carcinoma RNA-seq Hippo yes-associated protein

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yes-associated protein promotes endothelial-tomesenchymal transition of endothelial cells in choroidal neovascularization fibrosis

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International Journal of Ophthalmology(English edition) 2022年第5期15卷 701-710页

作者： Rong Zou Yi-Fan Feng Ya-Hui Xu Min-Qian Shen Xi Zhang Yuan-Zhi Yuan Department of Ophthalmology Zhongshan HospitalFudan UniversityShanghaiChina Department of Ophthalmology Xiamen BranchZhongshan HospitalFudan UniversityXiamenFujian ProvinceChina

AIM:To reveal whether and how yes-associated protein(YAP)promotes the occurrence of subretinal fibrosis in agerelated macular degeneration(AMD).METHODS:Cobalt chloride(Co Cl2)was used in primary human umbilical vein endothelial cells(HUVECs)to induce hypoxia in vitro.Eight-week-old male C57 BL/6 J mice weighing 19-25 g were used for a choroidal neovascularization(CNV)model induced by laser photocoagulation in vivo.Expression levels of YAP,phosphorylated YAP,mesenchymal markers[αsmooth muscle actin(α-SMA),vimentin,and Snail],and endothelial cell markers(CD31 and zonula occludens 1)were measured by Western blotting,quantitative real-time PCR,and immunofluorescence microscopy.Small molecules YC-1(Lificiguat,a specific inhibitor of hypoxia-inducible factor 1α),CA3(CIL56,an inhibitor of YAP),and XMU-MP-1(an inhibitor of Hippo kinase MST1/2,which activates YAP)were used to explore the underlying mechanism.RESULTS:Co Cl2 increased expression of mesenchymal markers,decreased expression of endothelial cell markers,and enhanced the ability of primary HUVECs to proliferate and migrate.YC-1 suppressed hypoxia-induced endothelialto-mesenchymal transition(End MT).Moreover,hypoxia promoted total expression,inhibited phosphorylation,and enhanced the transcriptional activity of YAP.XMU-MP-1 enhanced hypoxia-induced End MT,whereas CA3 elicited the opposite effect.Expression of YAP,α-SMA,and vimentin were upregulated in the laser-induced CNV model.However,silencing of YAP by vitreous injection of small interfering RNA targeting YAP could reverse these changes.CONCLUSION:The findings reveal a critical role of the hypoxia-inducible factor-1α(HIF-1α)/YAP signaling axis in End MT and provide a new therapeutic target for treatment of subretinal fibrosis in AMD.

关键词： endothelial-to-mesenchymal transition yes-associated protein hypoxia-inducible factor-1α choroidal neovascularization age-related macular degeneration

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Constitutive androstane receptor induced-hepatomegaly and liver regeneration is partially via yes-associated protein activation

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Acta Pharmaceutica Sinica B 2021年第3期11卷 727-737页

作者： Yue Gao Shicheng Fan Hua Li Yiming Jiang Xinpeng Yao Shuguang Zhu Xiao Yang Ruimin Wang Jianing Tian Frank JGonzalez Min Huang Huichang Bi Guangdong Provincial Key Laboratory of New Drug Design and Evaluation School of Pharmaceutical SciencesSun Yat-sen UniversityGuangzhou 510006China Department of Hepatic Surgery the Third Affiliated HospitalSun Yat-sen UniversityGuangzhou 510006China Laboratory of Metabolism Center for Cancer ResearchNational Cancer InstituteNIHBethesdaMD 20892USA

The constitutive androstane receptor(CAR, NR3 I1) belongs to nuclear receptor superfamily.It was reported that CAR agonist TCPOBOP induces hepatomegaly but the underlying mechanism remains largely unknown. yes-associated protein(YAP) is a potent regulator of organ size. The aim of this study is to explore the role of YAP in CAR activation-induced hepatomegaly and liver regeneration.TCPOBOP-induced CAR activation on hepatomegaly and liver regeneration was evaluated in wildtype(WT) mice, liver-specific YAP-deficient mice, and partial hepatectomy(PHx) mice. The results demonstrate that TCPOBOP can increase the liver-to-body weight ratio in wild-type mice and PHx mice.Hepatocytes enlargement around central vein(CV) area was observed, meanwhile hepatocytesproliferation was promoted as evidenced by the increased number of KI67+cells around portal vein(PV)area. The protein levels of YAP and its downstream targets were upregulated in TCPOBOP-treated mice and YAP translocation can be induced by CAR activation. Co-immunoprecipitation results suggested a potential proteineprotein interaction of CAR and YAP. However, CAR activation-induced hepatomegaly can still be observed in liver-specific YAP-deficient(Yape/e) mice. In summary, CAR activation promotes hepatomegaly and liver regeneration partially by inducing YAP translocation and interaction with YAP signaling pathway, which provides new insights to further understand the physiological functions of CAR.

关键词： Constitutive androstane receptor Nuclear receptors Hepatomegaly Liver enlargement Liver regeneration yes-associated protein proteineprotein interaction Partial hepatectomy

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Chinese Medical Journal 2021年第17期134卷 2054-2065页

作者： Bin Chen Bin Liu Tao Yu Yun-Feng Han Chao Wu Zhen-Yu Wang Department of Neurosurgery Peking University Third HospitalBeijing 100191China

Background:The Nuclear Dbf2-related(NDR1)kinase is a member of the NDR/LATS family,which was a supplementary of Hippo pathway.However,whether NDR1 could inhibit glioblastoma(GBM)growth by phosphorylating yes-associated protein(YAP)remains unknown.Meanwhile,the role of NDR1 in GBM was not clear.This study aimed to investigate the role of NDR1-YAP pathway in GBM.Methods:Bioinformation analysis and immunohistochemistry(IHC)were performed to identify the expression of NDR1 in GBM.The effect of NDR1 on cell proliferation and cell cycle was analyzed utilizing CCK-8,clone formation,immunofluorescence and flow cytometry,respectively.In addition,the xenograft tumor model was established as well.protein interaction was examined by Coimmunoprecipitation and immunofluorescence to observe co-localization.Results:Bioinformation analysis and IHC of our patients’tumor tissues showed that expression of NDR1 in tumor tissue was relatively lower than that in normal tissues and was positively related to a lower survival rate.NDR1 could markedly reduce the proliferation and colony formation of U87 and U251.Furthermore,the results of flow cytometry showed that NDR1 led to cell cycle arrest at the G1 phase.Tumor growth was also inhibited in xenograft nude mouse models in NDR1-overexpression group.Western blotting and immunofluorescence showed that NDR1 could integrate with and phosphorylate YAP at S127 site.Meanwhile,NDR1 could mediate apoptosis process.Conclusion:In summary,our findings point out that NDR1 functions as a tumor suppressor in GBM.NDR1 is identified as a novel regulator of YAP,which gives us an in-depth comprehension of the Hippo signaling pathway.

关键词： Glioblastoma Hippo signaling pathway Nuclear Dbf2-related yes-associated protein

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yes-associated protein contributes to magnesium alloy-derivedinflammation in endothelial cells

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Regenerative Biomaterials 2022年第1期9卷 130-142页

作者： Hongchi Yu Zhe Hou Nuoya Chen Rifang Luo Li Yang Michael Miao Xiaoyi Ma Lifeng Zhou Fugui He Yang Shen Xiaoheng Liu Yunbing Wang National Engineering Research Center for Biomaterials Sichuan UniversityChengdu 610065China Institute of Biomedical Engineering West China School of Basic Medical Sciences&Forensic MedicineSichuan UniversityChengdu 610041China Division of Oral&Craniofacial Health Sciences University of North Carolina Adams School of DentistryChapel HillNC 27599USA Beijing Key Laboratory of Cardiac Drug Device Technology and Evidence Based Medicine Beijing 100021China

Magnesium alloy(Mg alloy)has attracted massive attention in the potential applications of cardiovascular stents because of its good biocompatibility and degradability.However,whether and how the Mg alloy induces inflammation in endothelial cells remains unclear.In the present work,we investigated the activation of yes-associated protein(YAP)upon Mg alloy stimuli and unveiled the transcriptional function in Mg alloy-induced inflammation.Quantitative RT–PCR,western blotting and immunofluorescence staining showed that Mg alloy inhibited the Hippo pathway to facilitate nuclear shuttling and activation of YAP in human coronary artery endothelial cells(HCAECs).Chromatin immunoprecipitation followed sequencing was carried out to explore the transcriptional function of YAP in Mg alloy-derived inflammation.This led to the observation that nuclear YAP further bonded to the promoter region of inflammation transcription factors and co-transcription factors.This binding event activated their transcription and modified mRNA methylation of inflammation-related genes through regulating the expression of N6-methyladenosine modulators(METTL3,METTL14,FTO and WTAP).This then promoted inflammation-related gene expression and aggravated inflammation in HCAECs.In YAP deficiency cells,Mg alloy-induced inflammation was reduced.Collectively,our data suggest that YAP contributes to the Mg alloy-derived inflammation in HCAECs and may provide a potential therapeutic target that alleviates inflammation after Mg alloy stent implantation.

关键词： magnesium alloy yes-associated protein inflammation

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YAP regulates the liver size during the fasting-refeeding transition in mice

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Acta Pharmaceutica Sinica B 2023年第4期13卷 1588-1599页

作者： Xuan Li Shicheng Fan Chenghui Cai Yue Gao Xinhui Wang Yifei Zhang Hangfei Liang Huilin Li Jie Yang Min Huang Huichang Bi Guangdong Provincial Key Laboratory of New Drug Design and Evaluation School of Pharmaceutical SciencesSun Yat-sen UniversityGuangzhou 510006China NMPA Key Laboratory for Research and Evaluation of Drug Metabolism&Guangdong Provincial Key Laboratory of New Drug Screening School of Pharmaceutical SciencesSouthern Medical UniversityGuangzhou 510515China School of Pharmaceutical Sciences(Shenzhen) Sun Yat-sen UniversityShenzhen 518000China

Liver is the central hub regulating energy metabolism during feeding-fasting transition.Evidence suggests that fasting and refeeding induce dynamic changes in liver size,but the underlying mechanisms remain unclear.yes-associated protein(YAP)is a key regulator of organ size.This study aims to explore the role of YAP in fasting-and refeeding-induced changes in liver size.Here,fasting significantly reduced liver size,which was recovered to the normal level after refeeding.Moreover,hepatocyte size was decreased and hepatocyte proliferation was inhibited after fasting.Conversely,refeeding promoted hepatocyte enlargement and proliferation compared to fasted state.Mechanistically,fasting or refeeding regulated the expression of YAP and its downstream targets,as well as the proliferation-related protein cyclin D1(CCND1).Furthermore,fasting significantly reduced the liver size in AAV-control mice,which was mitigated in AAV Yap(5SA)mice.Yap overexpression also prevented the effect of fasting on hepatocyte size and proliferation.Besides,the recovery of liver size after refeeding was delayed in AAV Yap shRNA mice.Yap knockdown attenuated refeeding-induced hepatocyte enlargement and proliferation.In summary,this study demonstrated that YAP plays an important role in dynamic changes of liver size during fasting-refeeding transition,which provides new evidence for YAP in regulating liver size under energy stress.

关键词： Liver Fasting Refeeding yes-associated protein Hepatocyte size Hepatocyte proliferation β-Catenin Cyclin D1

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Survivin和yes-associated protein在宫颈癌组织中的表达及临床意义

Survivin和Yes-associated protein在宫颈癌组织中的表达及临床意...

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作者：谢颖芳大连医科大学

学位级别：硕士

目的: 检测正常宫颈、宫颈上皮内瘤样病变及宫颈癌组织中Survivin和yes-associated protein的表达水平,分析二者表达的差异性和相关性,探讨Survivin和yes-associated protein的表达与宫颈癌发生、发展的关系和临床意义。方法: ... 详细信息

目的: 检测正常宫颈、宫颈上皮内瘤样病变及宫颈癌组织中Survivin和yes-associated protein的表达水平,分析二者表达的差异性和相关性,探讨Survivin和yes-associated protein的表达与宫颈癌发生、发展的关系和临床意义。方法: 临床病理资料收集:收集大连医科大学附属第一医院妇产科手术切除宫颈上皮内瘤样病变及宫颈癌标本83例。其中宫颈上皮内瘤样病变（Cervical intraepithelial neoplasia,CIN）21例,浸润癌62例。浸润癌按FIGO分期:Ia期10例、Ib期31例、IIa期17例、IIb期4例;按WHO组织病理学分类:鳞癌49例,腺癌13例。同时选取子宫肌瘤患者子宫全切的正常宫颈组织15例作为对照。免疫组化染色与结果判定:采用免疫组织化学PV-6000-G二步法染色。Survivin阳性表达定位于细胞浆,偶见于细胞核,以细胞浆或胞核出现淡黄色、棕黄色或棕褐色颗粒为阳性信号;YAP阳性表达以在胞核或细胞浆出现淡黄色、棕黄色或棕褐色免疫反应颗粒为阳性信号。每例均随机观察5个高倍视野（×400）,用半定量积分法判断结果。染色阳性细胞所占比例按以下标准计分:阳性细胞≤5%为0分,6%～25%为1分,26%～50%为2分,51%～75%为3分,＞75%为4分;染色强度计分以细胞显色反应程度计分:无着色0分,淡黄色为1分,棕黄色为2分,棕褐色为3分;最后将阳性细胞所占的百分比分值和染色强度分值相乘为结果:0分为阴性（-）,1～4分为弱阳性（+）,5～8分为中度阳性（++）,9～l2分为强阳性（+++）。结果: 本研究实验结果表明Survivin在CIN和宫颈浸润癌中的阳性表达率显著高于正常宫颈组织,P＜0.01;在CIN和宫颈浸润癌之间Survivin的阳性表达率也有显著差异,P＜0.05,而且随着宫颈浸润癌临床分期的增高和组织分化程度的降低,Survivin的阳性表达率也增高,P＜0.05。宫颈腺癌中Survivin的阳性表达率显著高于鳞癌,P＜0.05。Survivin的阳性表达与患者的年龄无关,P＞0.05。 YAP在CIN和宫颈浸润癌中的阳性表达率显著高于正常宫颈组织,P＜0.05;但在CIN和宫颈浸润癌之间YAP的阳性表达率无显著差异,P＞0.05,随着宫颈癌临床分期的增高,YAP的阳性表达率也增高,但差别无统计学意义,P＞0.05。YAP的阳性表达与患者的年龄、组织类型以及分化程度无关,P＞0.05。 Survivin和YAP在宫颈癌组织中的表达呈正相关,r=0.323,P＜0.05。结论: Survivin的表达在CIN和宫颈浸润癌中显著高于正常宫颈组织,与宫颈癌的临床分期、组织类型和分化程度有关,与患者的年龄无关。提示Survivin在宫颈癌的发生、发展和组织侵袭中起了重要作用。 YAP在CIN和宫颈浸润癌中的阳性表达率显著高于正常宫颈组织,但与患者的年龄、临床分期、组织类型以及分化程度无关。推测YAP表达增高可能是宫颈上皮发生癌变的早期因素,应用免疫组化技术检测YAP蛋白在宫颈上皮的表达,有可能成为临床早期评价宫颈癌形成的重要分子生物学指标。 Survivin和YAP在宫颈癌组织中表达成正相关,YAP可能诱导凋亡抑制因子Survivin等的高表达,Survivin通过抑制宫颈癌中细胞凋亡、调节细胞有丝分裂和促进肿瘤血管形成等机制参与宫颈癌的发生、发展及转移。进一步研究Survivin和YAP之间关系与宫颈癌的形成机制,对指导宫颈癌的诊断、治疗和判断预后可提供更有效的理论依据。

关键词：宫颈癌 Survivin yes-associated protein 免疫组化

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Adaptable hydrogel with reversible linkages for regenerative medicine:Dynamic mechanical microenvironment for cells

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Bioactive Materials 2021年第5期6卷 1375-1387页

作者： Zongrui Tong Lulu Jin Joaquim Miguel Oliveira Rui LReis Qi Zhong Zhengwei Mao Changyou Gao MOE Key Laboratory of Macromolecular Synthesis and Functionalization Department of Polymer Science and EngineeringZhejiang UniversityHangzhou310027China 3B’s Research Group I3Bs-Research Institute on BiomaterialsBiodegradables and BiomimeticsUniversity of MinhoHeadquarters of the European Institute of Excellence on Tissue Engineering and Regenerative MedicineAveParkZona Industrial da Gandra4805-017Barco GMRPortugal ICVS/3B’s-PT Government Associate Laboratory Braga/GuimarãesPortugal The Discoveries Centre for Regenerative and Precision Medicine Headquarters at University of MinhoAvepark4805-017BarcoGuimarãesPortugal Key Laboratory of Advanced Textile Materials&Manufacturing Technology Ministry of EducationNational Base for International Science and Technology Cooperation in Textiles and Consumer-Goods ChemistryZhejiang Sci-Tech University310018HangzhouChina

Hydrogels are three-dimensional platforms that serve as substitutes for native extracellular matrix.These materials are starting to play important roles in regenerative medicine because of their similarities to native matrix in water content and flexibility.It would be very advantagoues for researchers to be able to regulate cell behavior and fate with specific hydrogels that have tunable mechanical properties as biophysical cues.Recent developments in dynamic chemistry have yielded designs of adaptable hydrogels that mimic dynamic nature of extracellular matrix.The current review provides a comprehensive overview for adaptable hydrogel in regenerative medicine as follows.First,we outline strategies to design adaptable hydrogel network with reversible linkages according to previous findings in supramolecular chemistry and dynamic covalent chemistry.Next,we describe the mechanism of dynamic mechanical microenvironment influence cell behaviors and fate,including how stress relaxation influences on cell behavior and how mechanosignals regulate matrix remodeling.Finally,we highlight techniques such as bioprinting which utilize adaptable hydrogel in regenerative medicine.We conclude by discussing the limitations and challenges for adaptable hydrogel,and we present perspectives for future studies.

关键词： Adaptable hydrogel Dynamic mechanical microenvironment Supramolecular chemistry Dynamic covalent chemistry yes-associated protein

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