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http://purl.uniprot.org/citations/35982896http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/35982896http://www.w3.org/2000/01/rdf-schema#comment"Senile osteoporosis is one of the major health problems in an aging society. Decreased bone formation due to osteoblast dysfunction may be one of the causes of aging-related bone loss. With increasing evidence suggesting that multiple microRNAs (miRNAs) play important roles in osteoblast function, the relationship between miRNAs and senile osteoporosis has become a popular research topic. Previously, we confirmed that mechanoresponsive miR-138-5p negatively regulated bone anabolic action. In this study, the miR-138-5p level was found to be negatively correlated with BMD and osteogenic markers in bone specimens of senile osteoporotic patients by bioinformatic analysis and experimental verification. Furthermore, high miR-138-5p levels aggravated the decrease of aged osteoblast differentiation in vitro and led to worse bone loss in aged osteoblastic miR-138-5p transgenic mice in vivo. We also previously identified that the target of miR-138-5p, microtubule actin cross-linking factor 1 (MACF1), could attenuate senile osteoporosis. Here, miR-138-5p was demonstrated to regulate aged osteoblast differentiation by targeting MACF1. Finally, the therapeutic inhibition of miR-138-5p counteracted the decrease in bone formation and aging-related bone loss in aged mice. Overall, our results highlight the crucial roles and the molecular mechanism of miR-138-5p in aging-related bone loss and may provide a powerful therapeutic target for ameliorating senile osteoporosis."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.org/dc/terms/identifier"doi:10.7150/ijbs.71411"xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Chen Z."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Chen X."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Chen G."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Deng X."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Li Y."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Lin X."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Li D."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Liu S."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Zhang Y."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Zhang G."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Wang X."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Xu X."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Yang C."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Zhao F."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Yin C."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Hu L."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Mao W."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Peng S."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Qian A."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Ru K."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/author"Huai Y."xsd:string
http://purl.uniprot.org/citations/35982896http://purl.uniprot.org/core/date"2022"xsd:gYear