ArticleTissue engineering. Part A2024
Porous Precision-Templated 40 μm Pore Scaffolds Promote Healing through Synergy in Macrophage Receptor with Collagenous Structure and Toll-Like Receptor Signaling.
Article in Tissue engineering. Part A, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Dual-Frequency Ultrasound Enhances Cavitation of Microdroplets for Controlled Scaffold Porosity in Tissue Engineering.ACS applied materials & interfaces · 2026Article
- Immunomodulatory Delivery Materials for Tissue Repair.Advanced healthcare materials · 2025Review
- Biomimetic Gradient Microporous Scaffold with a Triply Periodic Minimal Surface Enhances Osseointegration by Modulating Macrophage Polarization.Biomaterials research · 2025Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Porous precision-templated scaffolds (PTS) with uniform, interconnected, 40 μm pores have shown favorable healing outcomes and a reduced foreign body reaction (FBR). Macrophage receptor with collagenous structure (MARCO) and toll-like receptors (TLRs) have been identified as key surface receptors in the initial inflammatory phase of wound healing. However, the role of MARCO and TLRs in modulating monocyte and macrophage phenotypes within PTS remains uncharacterized. In this study, we demonstrate a synergetic relationship between MARCO and TLR signaling in cells inhabiting PTS, where induction with TLR3 or TLR4 agonists to 40 μm scaffold-resident cells upregulates the transcription of MARCO. Upon deletion of MARCO, the prohealing phenotype within 40 μm PTS polarizes to a proinflammatory and profibrotic phenotype. Analysis of downstream TLR signaling shows that MARCO is required to attenuate nuclear factor kappa B (NF-κB) inflammation in 40 μm PTS by regulating the transcription of inhibitory NFKB inhibitor alpha (
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.