ArticleMaterials today. Bio2024
Stiffness and surface topology of silicone implants competitively mediate inflammatory responses of macrophages and foreign body response.
Article in Materials today. Bio, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Mechano-immunomodulatory biomaterials: From immune mechanosensing to translational design.Bioactive materials · 2026Review
- Immune-epigenetic convergence in biomaterial-guided tissue regeneration.Materials today. Bio · 2026Article
- Inflammatory myofibroblasts reprogram neutrophil fate to drive chronic inflammation in peri-implantitis.International journal of oral science · 2026Article
- Targeting delayed healing tissues: immune reprogramming of adaptive immune cells by biomaterials.Regenerative biomaterials · 2026Review
- Advances in Silicone Implants Characterization: A Comprehensive Overview of Chemical, Physical and Biological Methods for Biocompatibility Assessment.Bioengineering (Basel, Switzerland) · 2025Review
- TLR4/NF-κB-mediated M1 macrophage polarization contributes to the promotive effects of ETS2 on ulcerative colitis.European journal of medical research · 2025Article
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Authors and funding
11 authors.
Funding
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Abstract
Adverse inflammatory responses, dominated by macrophages, that are induced by physical cues of silicone implants can heavily damage the life quality of patients via causing fibrosis and device failure. As stiffness and surface topology affect macrophages at the same time, the competition or partnership among physical cues against the regulation of macrophages is still ambiguous. Herein, a series of PDMS implants with different stiffness at ∼ MPa and surface topology at tens of micrometers were fabricated to investigate the relationship, the regulation rule, and the underlying mechanism of the two physical cues against the inflammatory responses of M1 macrophages. There is a competitive rule: surface topology could suppress the inflammatory responses of M1 macrophages in the soft group but did not have the same effect in the stiff group. Without surface topology, lower stiffness unexpectedly evoked stronger inflammatory responses of M1 macrophages. Implanting experiments also proved that the competitive state against mediating
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