文献类型：期刊文献

英文题名：A sulfated chitosan-driven immune-ECM reprogramming strategy to break the vicious cycle of aged wound healing

作者：Zhang, Xiaohui[1,2];Wang, Siyi[1,2];Liu, Yongqing[1,2];Wang, Jing[1,2,3];Liu, Changsheng[2,3]

机构：[1]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]East China Univ Sci & Technol, Engn Res Ctr Biomed Mat, Sch Mat Sci & Engn, Minist Educ, Shanghai 200237, Peoples R China;[3]East China Univ Sci & Technol, Frontiers Sci Ctr Materiobiol & Dynam Chem, Shanghai 200237, Peoples R China

年份：2026

卷号：64

起止页码：848

外文期刊名：BIOACTIVE MATERIALS

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001803299900001)】；

基金：This research was supported by the Excellence Research Group Program (No. T2288102), the Key Program of the National Natural Science Foundation of China (No. 32230059), the National Natural Science Foundation of China (No. 32471406), the Foundation of Frontiers Science Center for Materiobiology and Dynamic Chemistry (JKVD1211002) and Shandong Province key research and development project 2023CXPT103.r (2026) Program (No. T2288102) , the Key Program of the National Natural Science Foundation of China (No. 32230059) , the National Natural Science Foundation of China (No. 32471406) , the Foundation of Frontiers Science Center for Materiobiology and Dynamic Chemistry (JKVD1211002) and Shandong Province key research and development project 2023CXPT103.

语种：英文

外文关键词：Sulfated chitosan; Synthetic glycosaminoglycan; Macrophage polarization; Extracellular matrix degradation; Sulfonate groups; Aged wound healing

摘要：Chronic wounds in the elderly are characterized by persistent inflammation and excessive extracellular matrix (ECM) degradation, which form a self-perpetuating vicious cycle that impedes healing and increases morbidity. Here, we identify sulfated chitosan (SCS) as an a synthetic glycosaminoglycan capable of disrupting this pathological "ECM degradation-immune imbalance" cycle and promoting robust skin wound repair in aged mice. SCS activates JAK2-STAT3/STAT6 signaling to rebalance M1/M2 macrophage polarization, while simultaneously enhancing phosphoadenosine phosphosulfate (PAPS) production and sulfonate-group trafficking. These coordinated actions collectively improved collagen deposition, angiogenesis, and glycosaminoglycan (GAG) content within the wound microenvironment. Using Sulf2 knockdown and overexpression models, we further show that chitosan-anchored sulfonate groups are required for driving macrophages toward an M2 phenotype, whereas free sulfonate groups facilitate glycosaminoglycan biosynthesis. These coordinated immune and matrix effects lead to enhanced collagen organization, angiogenesis, and glycosaminoglycan deposition within the aged wound microenvironment.Together, this work establishes SCS as a materials-driven immune-ECM reprogramming strategy and highlights its translational potential for the treatment of age-associated chronic wounds.