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Mechanistically, ferroptosis in transplanted hearts triggers the initial release of DAMPs, which bind to endothelial Toll-like receptor 4 (TLR4) and stimulate type I interferon production via Trif-mediated signaling, promoting the recruitment of neutrophils to the injured heart [103]
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2.3 Stimuli-responsive and targeting modules as functional units Building on this scaffold, endogenous and exogenous stimuli-responsive elements together with active targeting modules provide ways to focus nanocarrier action on specific TME regions or cell populations [46,47,48]
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