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Nanomedicine platforms offer precise tools for macrophage modulation, enabling the targeted delivery of polarization-inducing agents directly to the TME while sparing peripheral tissues (4750)accompanied by the robust activation of the NF-B and STAT1 pathways that drive the transcription of pro-inflammatory cytokines and immunostimulatory factors (51, 52)
The mechanism of GSH-mediated biofilm disruption is possibly due to a concentration-dependent increase in GSH acidity that triggers cleaving of the matrix components
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GLP-1RAs prevent post-MI remodeling by having an impact on the extracellular matrix changes rather than dependency on its glycemic control [76]
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