Transcriptomic profiling of Guanxin Shuxin powder effects on a mouse model of coronary microvascular dysfunction
Biological Relevance and Intent Coronary microvascular dysfunction (CMD) is a major driver of myocardial ischemia, yet therapeutic options remain limited. This study aims to evaluate the cardioprotective efficacy of Guanxin Shuxin powder (GXSX), a traditional Chinese medicine, and to elucidate its underlying molecular mechanisms. The research specifically investigates how GXSX modulates metabolic pathways and preserves mitochondrial ultrastructure to improve coronary microvascular perfusion and cardiac function. Experimental Workflow The experimental approach integrated physiological assessment, histopathology, and high-throughput sequencing: In Vivo Model: A mouse model of CMD was established and treated with GXSX. Phenotypic Validation: Cardiac function was monitored via echocardiography, while coronary perfusion and myocardial architecture were assessed using CD31 immunofluorescence and histopathological staining. Molecular Profiling: Bulk RNA-sequencing was performed on myocardial tissues to identify differentially expressed genes and enriched metabolic pathways. Mechanism Verification: Candidate targets (notably MDH1) and downstream markers of oxidative stress and ferroptosis (GPX4, 4-HNE) were validated through metabolic assays and protein expression profiling. Ultrastructural Analysis: Transmission electron microscopy (TEM) was utilized to observe mitochondrial morphological changes in response to treatment.
Biological Relevance and Intent Coronary microvascular dysfunction (CMD) is a major driver of myocardial ischemia, yet therapeutic options remain limited. This study aims to evaluate the cardioprotective efficacy of Guanxin Shuxin powder (GXSX), a traditional Chinese medicine, and to elucidate its underlying molecular mechanisms. The research specifically investigates how GXSX modulates metabolic pathways and preserves mitochondrial ultrastructure to improve coronary microvascular perfusion and cardiac function. Experimental Workflow The experimental approach integrated physiological assessment, histopathology, and high-throughput sequencing: In Vivo Model: A mouse model of CMD was established and treated with GXSX. Phenotypic Validation: Cardiac function was monitored via echocardiography, while coronary perfusion and myocardial architecture were assessed using CD31 immunofluorescence and histopathological staining. Molecular Profiling: Bulk RNA-sequencing was performed on myocardial tissues to identify differentially expressed genes and enriched metabolic pathways. Mechanism Verification: Candidate targets (notably MDH1) and downstream markers of oxidative stress and ferroptosis (GPX4, 4-HNE) were validated through metabolic assays and protein expression profiling. Ultrastructural Analysis: Transmission electron microscopy (TEM) was utilized to observe mitochondrial morphological changes in response to treatment.
European Bioinformatics Institute