This review explores the role of pyroptosis in diabetic cardiomyopathy (DCM). DCM is a common complication of diabetes, characterized by structural and functional abnormalities in the heart. Recent studies suggest that pyroptosis, a form of programmed cell death associated with inflammation, exacerbates DCM. The review summarizes the mechanisms by which pyroptosis contributes to DCM and discusses potential therapeutic strategies targeting pyroptosis. Key mechanisms include the NLRP3 inflammasome-mediated pyroptosis, different pyroptosis pathways in DCM, and the effects of pyroptosis in various cell types. The review also highlights potential drugs targeting the NLRP3 inflammasome/pyroptosis for DCM treatment. Pyroptosis is involved in the progression of DCM through chronic inflammation, oxidative stress, and cellular death. The review discusses the role of various pathways, including the NF-κB/NLRP3 inflammasome pathway, reactive oxygen species/thioredoxin interacting protein/NLRP3 inflammasome pathway, and Nrf2-related pathways. The review also examines the effects of pyroptosis in cardiomyocytes, macrophages, fibroblasts, and vascular endothelial cells on DCM. Potential therapies include hypoglycemic drugs, inhibitors of the NLRP3 inflammasome, and non-coding RNAs. The review concludes that understanding pyroptosis mechanisms may provide new therapeutic targets for DCM.This review explores the role of pyroptosis in diabetic cardiomyopathy (DCM). DCM is a common complication of diabetes, characterized by structural and functional abnormalities in the heart. Recent studies suggest that pyroptosis, a form of programmed cell death associated with inflammation, exacerbates DCM. The review summarizes the mechanisms by which pyroptosis contributes to DCM and discusses potential therapeutic strategies targeting pyroptosis. Key mechanisms include the NLRP3 inflammasome-mediated pyroptosis, different pyroptosis pathways in DCM, and the effects of pyroptosis in various cell types. The review also highlights potential drugs targeting the NLRP3 inflammasome/pyroptosis for DCM treatment. Pyroptosis is involved in the progression of DCM through chronic inflammation, oxidative stress, and cellular death. The review discusses the role of various pathways, including the NF-κB/NLRP3 inflammasome pathway, reactive oxygen species/thioredoxin interacting protein/NLRP3 inflammasome pathway, and Nrf2-related pathways. The review also examines the effects of pyroptosis in cardiomyocytes, macrophages, fibroblasts, and vascular endothelial cells on DCM. Potential therapies include hypoglycemic drugs, inhibitors of the NLRP3 inflammasome, and non-coding RNAs. The review concludes that understanding pyroptosis mechanisms may provide new therapeutic targets for DCM.