Novel enzyme-sensitive poly-tioxolone membranes for peritendinous anti-adhesion

Li, Yuange; Yu, Qing; Ling, Zemin; Chen, Hongqi; Liu, Xuanzhe; Wu, Tianyi; Hu, Bo; Fan, Cunyi; Jiang, Xuefeng; Liu, Shen

doi:10.1016/j.compositesb.2022.109904

Cited by 7 publications

(4 citation statements)

References 38 publications

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“…There are plenty of studies about influencing fibroblast and vascular formation to prevent POA, most of which are pure agents or combination of biomaterials and agents. Celecoxib [ 251 ], 5-nitro-2 -(3-phenylpropyl amino)-benzoic acid (NPPB) [ 252 ], tioxolone [ 253 ], p-glycoprotein (P-gp) inhibitor [ 254 ], l -phenylalanine (l-Phe) [ 255 ] and low concentrations of dexamethasone [ 256 ], etc. , have been demonstrated to inhibit the activity or proliferation of fibroblasts and decrease collagen secretion, performing prominent anti-adhesion potential without evident side effect.…”

Section: Possible Strategies For Preventing Adhesion By Using Biomate...mentioning

confidence: 99%

Prevention strategies of postoperative adhesion in soft tissues by applying biomaterials: Based on the mechanisms of occurrence and development of adhesions

Liao

Fan

2023

Bioactive Materials

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Section: Possible Strategies For Preventing Adhesion By Using Biomate...mentioning

confidence: 99%

Prevention strategies of postoperative adhesion in soft tissues by applying biomaterials: Based on the mechanisms of occurrence and development of adhesions

Liao

Fan

2023

Bioactive Materials

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“…In addition, the presence of large amounts of lipase and MMP2 was demonstrated in peritendinous tissue during the proliferative and remodeling phases. To utilize this feature, Li et al fabricated a polymerized tioxolone-loaded barriers, in which the ester bond of polymerized drug can be hydrolyzed by lipase to convert into monomer in responsive releasing profile for subsequent anti-adhesion in repair site [92] . Cai et al also synthesized MMP2 responsive unidirectional hydrogel-electrospun patch to release TGF-β1 siRNA in MMP-2 overexpression microenvironment to achieve adhesion prevention [82] .…”

Section: Therapeutic Intervention Of Pamentioning

confidence: 99%

Peritendinous adhesion: Therapeutic targets and progress of drug therapy

Wang,

Sha,

Zhao

et al. 2024

Computational and Structural Biotechnology Journal

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“…Along with the tendon healing, the peritendinous adhesion is formed by excessive invasion of granulation tissue from surrounding tissues. 3 , 4 Recently, the well-known intricate process of tendon adhesion formation is driven by the interaction among various peritendinous cell lineages, encompassing immune, endothelial, and mesenchymal cells. 5 These cells are found within specialized fibrotic areas, referred to as the fibrotic niche.…”

Section: Introductionmentioning

confidence: 99%

Multi-omics analysis of human tendon adhesion reveals that ACKR1-regulated macrophage migration is involved in regeneration

Zhang,

Xiao,

et al. 2024

Bone Res

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Tendon adhesion is a common complication after tendon injury with the development of accumulated fibrotic tissues without effective anti-fibrotic therapies, resulting in severe disability. Macrophages are widely recognized as a fibrotic trigger during peritendinous adhesion formation. However, different clusters of macrophages have various functions and receive multiple regulation, which are both still unknown. In our current study, multi-omics analysis including single-cell RNA sequencing and proteomics was performed on both human and mouse tendon adhesion tissue at different stages after tendon injury. The transcriptomes of over 74 000 human single cells were profiled. As results, we found that SPP1+ macrophages, RGCC+ endothelial cells, ACKR1+ endothelial cells and ADAM12+ fibroblasts participated in tendon adhesion formation. Interestingly, despite specific fibrotic clusters in tendon adhesion, FOLR2+ macrophages were identified as an antifibrotic cluster by in vitro experiments using human cells. Furthermore, ACKR1 was verified to regulate FOLR2+ macrophages migration at the injured peritendinous site by transplantation of bone marrow from Lysm-Cre;R26RtdTomato mice to lethally irradiated Ackr1−/− mice (Ackr1−/− chimeras; deficient in ACKR1) and control mice (WT chimeras). Compared with WT chimeras, the decline of FOLR2+ macrophages was also observed, indicating that ACKR1 was specifically involved in FOLR2+ macrophages migration. Taken together, our study not only characterized the fibrosis microenvironment landscape of tendon adhesion by multi-omics analysis, but also uncovered a novel antifibrotic cluster of macrophages and their origin. These results provide potential therapeutic targets against human tendon adhesion.

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Novel enzyme-sensitive poly-tioxolone membranes for peritendinous anti-adhesion

Cited by 7 publications

References 38 publications

Prevention strategies of postoperative adhesion in soft tissues by applying biomaterials: Based on the mechanisms of occurrence and development of adhesions

Prevention strategies of postoperative adhesion in soft tissues by applying biomaterials: Based on the mechanisms of occurrence and development of adhesions

Peritendinous adhesion: Therapeutic targets and progress of drug therapy

Multi-omics analysis of human tendon adhesion reveals that ACKR1-regulated macrophage migration is involved in regeneration

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