{"database":"iProX","file_versions":[],"scores":null,"additional":{"omics_type":["Proteomics"],"submitter":["Yiying Qi"],"species":["Mus Musculus"],"full_dataset_link":["http://www.iprox.org/page/project.html?id=IPX0012242000"],"submitter_email":["qiyiying@zju.edu.cn"],"submitter_affiliation":["Zhejiang University"],"sample_protocol":[""],"repository":["iProX"],"data_protocol":[""],"pubmed_abstract":["Senescent cells (SnCs) are increasingly recognized as key contributors to osteoarthritis, with conventional strategies centered on their elimination. However, senolytic approaches face mounting limitations, driving the need for refined interventions. Here, we exploit SnCs' lipid metabolic signature to develop a senotherapeutic strategy. Given the universal lipid accumulation in SnCs and the dual role of lipids as both metabolic liabilities and essential lubricants, we engineer an injectable nanoliposuction hydrogel platform designed for \"waste recycling\". This system removes excess lipids to mitigate senescence-associated secretory phenotype (SASP) propagation and incorporates the harvested lipids as a pivotal component of the biomimetic lubricating system, thereby alleviating mechanical allodynia and cartilage wear. This strategy circumvents potential side effects associated with direct SnCs clearance and repurposes these traditionally harmful cells as functional resources. Our findings establish a shift in the philosophy of senescence therapy, transitioning the focus from destructive ablation to spatially adaptive reallocation of metabolites."],"pubmed_title":["Recycling senescent cell lipids for targeted senotherapy."],"pubmed_authors":["Ji Xiaoxiao X, He Xingzi X, Cai Honglu H, Tang Peng P, Zhou Hao H, Wang Jiajie J, Wu Yifan Y, Zhou Jinfeng J, Lin Zhang Z, Xu Kaicheng K, Lin Changjian C, Wu Xiaoyong X, Wang Kanbin K, Liu Wangmi W, Feng Gang G, Yan Shigui S, Jiang Guangyao G, Qu Zihao Z, Qi Yiying Y"],"additional_accession":[]},"is_claimable":false,"name":"Nanoliposuction recycles senescent cell lipids for lubrication","description":"This study aims to systematically profile membrane protein alterations associated with chondrocyte senescence, in order to identify surface markers specifically upregulated in aged cartilage. We established two in vitro models by treating primary chondrocytes with IL-1β or bleomycin, and one in vivo model by comparing cartilage from young and aged mice. Membrane proteins were extracted and subjected to quantitative proteomic analysis.","dates":{"publication":"Tue Jun 10 00:00:00 GMT+01:00 2025"},"accession":"PXD064867","cross_references":{"TAXONOMY":["10090"],"pubmed":["41820407"]}}