TL;DR
Tβ4 exerts neuroprotective effects against ACI by suppressing the TLR4/NF-κB signaling pathway and mitigating neuronal pyroptosis and mitigating neuronal pyroptosis, demonstrating potential clinical application value.
Elevated endogenous BHB under obese conditions exerts neuroprotective effects against CIRI, and exogenous BHB can mimic this effect.
LRP5 deficiency aggravates cardiac injury and is associated with increased neuronal susceptibility to inflammatory signals, and cell type-specific roles for LRP5 in the inflammatory response to MI are revealed.
By inhibiting the JAK1/STAT1 pathway, BHB promotes microglia M2 polarization and enhances their phagocytosis, attenuates neuroinflammation and neuronal injury, and ultimately exerts anti-EP effects.
The findings suggest that STING is a promising therapeutic target for reducing neuroinflammation and neuronal damage, ultimately contributing to the alleviation of brain injury after CA.
Findings position C3aR-STING signaling as a complement-linked mechanism regulating ferroptosis and suggest a potential therapeutic direction for limiting reperfusion-associated injury after ischemic stroke.
Tar improved CIRI induced inflammation and ferroptosis through regulating the AKT/NF‐κB pathway and reversed the protective effects of Tar in OGD/R‐induced PC12 cells.
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