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您的检索式：作者名="Chunyang Mo"
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| 1 | Electroactive polymeric nanofibrous composite to drive in situ construction of lithiophilic SEI for stable lithium metal anodes显示文摘Uncontrolled lithium dendrite growth hinders the practical application of lithium metal batteries(LMBs).Herein,we report a novel Li^(+) flux distributor achieved by placing an electroactive polyvinylidene fluoride/polymethyl methacrylate(PVDF/PMMA)composite nanofiber interlayer on a current collector,inducing uniform lithium deposition to mitigate the dendrite problem.Specifically,the released PMMA reacts with Liþto form abundant C–O–Li bonds and generate in situ a stable lithiophilic PMMA-Li solid electrolyte interphase layer.Theoretical calculations reveal that polar C–F groups in the PVDF framework and lithiophilic PMMA-Li provide homo-dispersed Li^(+) migration pathways with low energy barriers.Consequently,uniform Li nucleation is achieved at the molecular level,resulting in ultrahigh cycling stability with dendrite-free Li deposition at 5 mA cm^(-2) and 5 mAh cm^(-2)for over 500 h.The PVDF/PMMA||Li||LiFePO_(4)(LFP)full cell presents an increased rate capacity of 110 mAh g^(-1) at 10 C.In addition,a soft-package battery demonstrates a high energy density of 289 Wh kg^(-1).This work provides a facile design for stable lithium metal anodes to promote the practical use of LMBs and other alkali metal batteries. | Ai-Long Chen Nan Shang Yue Ouyang Lulu Mo Chunyang Zhou Weng Weei Tjiu Feili Lai Yue-E Miao Tianxi Liu | 2022 | eScience2022，2，2： | 3 |
| 2 | Premature aging of skeletal stem/progenitor cells rather than osteoblasts causes bone loss with decreased mechanosensation显示文摘A distinct population of skeletal stem/progenitor cells(SSPCs)has been identified that is indispensable for the maintenance and remodeling of the adult skeleton.However,the cell types that are responsible for age-related bone loss and the characteristic changes in these cells during aging remain to be determined.Here,we established models of premature aging by conditional depletion of Zmpste24(Z24)in mice and found that Prx1-dependent Z24 deletion,but not Osx-dependent Z24 deletion,caused significant bone loss.However,Acan-associated Z24 depletion caused only trabecular bone loss.Single-cell RNA sequencing(sc RNA-seq)revealed that two populations of SSPCs,one that differentiates into trabecular bone cells and another that differentiates into cortical bone cells,were significantly decreased in Prx1-Cre;Z24^(f/f)mice.Both premature SSPC populations exhibited apoptotic signaling pathway activation and decreased mechanosensation.Physical exercise reversed the effects of Z24depletion on cellular apoptosis,extracellular matrix expression and bone mass.This study identified two populations of SSPCs that are responsible for premature aging-related bone loss.The impairment of mechanosensation in Z24-deficient SSPCs provides new insight into how physical exercise can be used to prevent bone aging. | Ruici Yang Dandan Cao Jinlong Suo Lingli Zhang Chunyang Mo Miaomiao Wang Ningning Niu Rui Yue Weiguo Zou | 2023 | Bone Research2023，11，3： | 0 |
| 3 | Inhibition of fibroblast activation protein ameliorates cartilage matrix degradation and osteoarthritis progression显示文摘Fibroblast activation protein(Fap)is a serine protease that degrades denatured type I collagen,α2-antiplasmin and FGF21.Fap is highly expressed in bone marrow stromal cells and functions as an osteogenic suppressor and can be inhibited by the bone growth factor Osteolectin(Oln).Fap is also expressed in synovial fibroblasts and positively correlated with the severity of rheumatoid arthritis(RA).However,whether Fap plays a critical role in osteoarthritis(OA)remains poorly understood.Here,we found that Fap is significantly elevated in osteoarthritic synovium,while the genetic deletion or pharmacological inhibition of Fap significantly ameliorated posttraumatic OA in mice.Mechanistically,we found that Fap degrades denatured type II collagen(Col II)and Mmp13-cleaved native Col II.Intra-articular injection of r Fap significantly accelerated Col II degradation and OA progression.In contrast,Oln is expressed in the superficial layer of articular cartilage and is significantly downregulated in OA.Genetic deletion of Oln significantly exacerbated OA progression,which was partially rescued by Fap deletion or inhibition.Intra-articular injection of r Oln significantly ameliorated OA progression.Taken together,these findings identify Fap as a critical pathogenic factor in OA that could be targeted by both synthetic and endogenous inhibitors to ameliorate articular cartilage degradation. | Aoyuan Fan Genbin Wu Jianfang Wang Laiya Lu Jingyi Wang Hanjing Wei Yuxi Sun Yanhua Xu Chunyang Mo Xiaoying Zhang Zhiying Pang Zhangyi Pan Yiming Wang Liangyu Lu Guojian Fu Mengqiu Ma Qiaoling Zhu Dandan Cao Jiachen Qin Feng Yin Rui Yue | 2023 | Bone Research2023，11，1： | 0 |
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