Similar to previous animal studies, we found that TLR4 overexpression reactivated downstream MyD88/NF-κB signaling, thereby upregulating the protein expression of caspase-1, NLRP3, HMGB-1, and GSDMD, as well as enhancing serum inflammatory factors in the Dox-HF group, as shown in Table 2. The gene discussed is CASP1; the disease is hydrops fetalis.