This study systematically reviewed the spectrum and applicability of rodent myocardial injury models, and proposes a selection and reporting framework of “ research question-mechanism-model-evaluationtranslation” to enhance their reproducibility and clinical translatability. Although numerous models have emerged,coronary artery ligation models that simulate myocardial infarction remain the cornerstone for investigating ischemic heart disease mechanisms and evaluating therapeutic strategies, because of their high fidelity in reproducing the pathophysiology, robust reproducibility, and stable replication of long-term outcomes such as ventricular remodeling.Considering ischemic, physical / chemical, pharmacological / inflammatory, and genetic models, we summarize the key procedural parameters, variable factors, and sources of bias, and integrate the morphological, functional, and molecular biomarker-based three-dimensional evaluation pathways. Permanent ligation is an appropriate strategy for studies of ventricular remodeling and chronic fibrosis, while ischemia-reperfusion closely mimics clinical reperfusion scenarios and reperfusion injury, and cryo- and thermal injury produce clearly demarcated focal lesions, facilitating repair, regeneration, and biomaterials evaluation. Isoproterenol-, doxorubicin-, and lipopolysaccharide-inducedmodels display phenotype specificity in relation to stress-induced necrosis, chemotherapy-related cardiotoxicity, and systemic inflammation, respectively, while genetic engineering models are advantageous for causal inference but involve higher costs and technical barriers. We recommend that models should be selected and combined according to the specific scientific questions, validated using stratified approaches, and accompanied by a minimal reporting checklist to reduce inter-experimental variability, strengthen the robustness of the evidence, and improve translational value.