Integrated single-cell transcriptomics and in vivo investigation reveal the role of ANXA1 in intestinal barrier dysfunction during heat stroke by mediating neutrophil-monocyte interaction and regulating the TLR4/ERK/NF-κB pathway.

and Ly6G. Apart from reversing the ANXA1 and FPR2 protein expression levels, inhibiting ANXA1 aggravated the damaging effects of HS on the colon tissue. In conclusion, ANXA1 protected against HS-induced intestinal barrier dysfunction by regulating neutrophil-monocyte interaction and inhibiting TLR4/ERK/NF-κB, with ANXA1-FPR2 as a key axis, which offers a novel target and strategy for the clinical treatment of HS-induced intestinal barrier dysfunction.