文献类型：期刊文献

英文题名：Programmable viscoelastic hydrogel enables factor-free adipogenesis of MSCs through mechanotransduction

作者：Li, Tianyue[1];Wang, Yanwen[2];Li, Ziyuan[1];Tan, Poh-Ching[2];Hu, Chenghuizi[1];Jin, Jiajun[1];Zhou, Shuang-Bai[2];Li, Qing-Feng[2];Zhang, Junji[1]

机构：[1]East China Univ Sci & Technol, Feringa Nobel Prize Scientist Joint Res Ctr, Frontiers Sci Ctr Materiobiol & Dynam Chem, Inst Fine Chem,Key Lab Adv Mat & Joint Int Res Lab, Shanghai 200237, Peoples R China;[2]Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Sch Med, Dept Plast & Reconstruct Surg, Shanghai, Peoples R China

年份：2026

卷号：535

外文期刊名：CHEMICAL ENGINEERING JOURNAL

收录：;EI(收录号：20261520490169);WOS:【SCI-EXPANDED(收录号:WOS:001737543300001)】；

基金：This work is supported by NSFC (22378121, 22105070, 82272287) , Science and Technology Commission of Shanghai Municipality (24DX1400200) , the Fundamental Research Funds for the Central Uni-versities (222201717003) . JZ acknowledges Shanghai Natural Science Foundation Project (23ZR1479500, 23JC1401700) . ZL acknowledges Shanghai Sailing Program (20YF1410300) . SZ acknowledges the Shanghai Key Research Center-Shanghai Research Center for Plastic Surgery (2023ZZ02023) .

语种：英文

外文关键词：Dynamic hydrogels; Mechanosensation; Adipogenesis; Stem cell; Extracellular matrix (ECM) mimetics

摘要：Mesenchymal stem cell (MSC) adipogenesis plays pivotal roles in physiological and pathological contexts, yet remains predominantly induced by biochemical factors in biomedical application. While viscoelastic microenvironments influence MSC fate, prior studies focus on osteogenesis, leaving adipogenic mechanotransduction poorly defined. To address this, we engineered a programmable viscoelastic hydrogel replicating soft tissue mechanics (modulus: 5-700 Pa; relaxation tau 1/2: 2-170 s). This platform enables on-demand control of adipogenic efficiency through tunable mechano-regulation of the microenvironment, achieving biochemical factor-free differentiation. Mechanistically, biomimetic viscoelasticity upregulates SFRP2, which suppresses Wnt/beta-catenin signaling as evidenced by reduced WNT5A and CTNNB1 expression and inhibited beta-catenin/YAP1 nuclear translocation. This cascade de-represses PPAR-gamma and activates adipogenic programs (C/EBP alpha/FABP4). Loss-offunction studies also confirm the causal role of SFRP2 in this pathway. Collectively, we uncover a mechanical regulation axis for adipogenesis and establish a tunable material platform for spatially controlled tissue engineering, advancing mechanics-directed regenerative strategies.