The abstract describes macrophage polarization as a phenotype switch from pro-inflammatory M1 to pro-resolving M2 states during oral wound healing.
First-pass extracted concept
macrophage polarization
Aliases
M1 to M2 phenotype switching
Extracted Explainers
What the tool is doing
What problem it solves
Evidence Snippets
Macrophages play a central role in this transition through phenotype switching from a pro-inflammatory (M1) to a pro-resolving, anti-inflammatory (M2) state.
By integrating insights into macrophage polarization, metabolic modulation, autophagy promotion, and cell death regulation, HDTs offer innovative and multifaceted approaches to TB treatment.
It also serves as a signaling molecule that modulates macrophage polarization between pro- and anti-inflammatory phenotypes in response to inflammatory and metabolic signals in their local environment.
Supporting Sources
Linked Claims
Macrophages play a central role in oral wound-healing transitions through switching from M1 to M2 states.
Macrophages play a central role in this transition through phenotype switching from a pro-inflammatory (M1) to a pro-resolving, anti-inflammatory (M2) state.
Microbiome-mediated signaling and macrophage plasticity critically interact to shape oral wound outcomes.
Emerging evidence highlights the critical interplay between microbiome-mediated signaling and macrophage plasticity in shaping wound outcomes, suggesting that similar mechanisms operate within the oral cavity.
Resolution of inflammation is necessary to promote tissue remodeling and functional regeneration in wound repair.
Inflammation is an essential component of wound repair, and its resolution is necessary to promote tissue remodeling and functional regeneration.
Lactate acts as a signaling molecule that modulates macrophage polarization between pro-inflammatory and anti-inflammatory phenotypes in response to local inflammatory and metabolic signals.
The review frames macrophage polarization, metabolic modulation, autophagy promotion, and cell death regulation as key host-directed therapy axes for tuberculosis treatment.
By integrating insights into macrophage polarization, metabolic modulation, autophagy promotion, and cell death regulation, HDTs offer innovative and multifaceted approaches to TB treatment.
Regulation by lactate and lactylation during macrophage polarization in sepsis may represent a potential therapeutic target for sepsis.