Abstract: Diabetic cardiomyopathy(DCM)refers to specific structural and functional myocardial abnormalities that develop independent of coronary artery disease,hypertension,or valvular disorders.Although all forms of diabetes can lead to myocardial injury,DCM associated with type 2 diabetes mellitus(T2DM)is the most prevalent and most extensively studied subtype.The onset and progression of DCM involve disturbances in energy metabolism,chronic inflammation,and immune dysregulation.In recent years,the gut microbiota—often referred to as the “second genome” —has been recognized as a pivotal modulator of the pathophysiological processes underlying DCM.This review systematically summarizes the structural and functional alterations of the gut microbiota observed in patients with T2DM and DCM,highlighting its regulatory roles through multiple metabolic and immune pathways,including the bile acid-farnesoid X receptor/Takeda G-protein receptor 5 axis,branched-chain amino acid metabolism-mitochondrial function coupling,trimethylamine N-oxide-mediated inflammatory signaling,the short-chain fatty acids/glucagon-like peptide-1/AMP-activated protein kinase pathway,and the tryptophan-indole-aryl hydrocarbon receptor axis,as well as mechanisms involving gut barrier disruption and endotoxemia.Furthermore,the potential involvement of non-bacterial microbial components—such as fungi,bacteriophages,and enteric viruses—in DCM pathogenesis is discussed,alongside recent advances in microbiota-targeted interventions including probiotics,prebiotics,and fecal microbiota transplantation.Future investigations employing large-scale,multicenter,and longitudinal designs combined with multi-omics analyses are warranted to elucidate the causal relationships and translational potential of the gut-heart axis,which will provide novel insights into the early prediction and precision management of DCM.

Key words: diabetic cardiomyopathy, gut microbiota, metabolites, inflammatory mechanisms, biomarkers