Mitochondrial quality control at the ferroptosis-pyroptosis interface in diabetic cardiomyopathy: a narrative critical synthesis.

Diabetic cardiomyopathy is clinically heterogeneous, whereas much of its mechanistic literature relies on experimental models. This narrative critical synthesis examines whether mitochondrial quality control links diabetic stress to ferroptosis, pyroptosis, and multicellular remodeling. The evidence base is an author-selected set of 112 publications mapped from a 400-record collection, supplemented by methodological and clinical context. Original database-specific search histories were not retained in the available materials. PubMed Central full text was available for 66 corpus records; 46 were initially accessible only as abstracts. A focused full-text reassessment of selected original reports replaces the earlier corpus-wide support labels. We distinguish core quality-control processes from associated metabolic regulators and separate death markers from functional evidence of execution. The best-supported findings concern model-specific changes in mitochondrial function, lipid-peroxide-sensitive injury, and intercellular communication. They do not establish a universal mitochondrial quality-control hierarchy or same-cell ferroptosis-pyroptosis co-execution. No single study identified in the available evidence demonstrates all three transitions from markers to execution, from one death program to another, and from rodents to a corresponding human mechanism. We compare same-cell coupling with cross-cell propagation and specify experiments that would distinguish them. Human phenotype and prognosis associations support disease relevance but cannot establish myocardial death mechanisms or therapeutic mediation. The resulting framework treats mitochondrial quality control as interacting, separable processes that may alter susceptibility to particular death programs, rather than as an established master regulator.