biostudies-arrayexpressUnknownTranscriptomicsGenomicsProteomicsShuai LiIllumina NovaSeq 6000RNA-seq of coding RNAMus musculusMus musculushttps://www.ebi.ac.uk/biostudies/studies/E-MTAB-17126Biological 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.biostudies-arrayexpressSequencing - The prepared libraries were sequenced on an Illumina NovaSeq 6000 platform to generate 150 bp paired-end reads. A minimum of 20 million raw reads were generated for each sample to ensure sufficient coverage for transcriptomic analysis.Sample Collection - At the end of the 4-week treatment period, mice were anesthetized. Following euthanasia, the heart tissues were rapidly excised, rinsed in ice-cold phosphate-buffered saline (PBS) to remove residual blood, and then immediately snap-frozen in liquid nitrogen and stored at -80°C until RNA extraction.Nucleic Acid Extraction - Total RNA was extracted from the frozen heart tissues using TRIzol reagent (Invitrogen, USA) following the manufacturer’s instructions. The concentration and purity of the extracted RNA were determined using a NanoDrop spectrophotometer, and RNA integrity was assessed using the Agilent 2100 Bioanalyzer (Agilent Technologies, USA).Library Construction - Sequencing libraries were generated using the NEBNext Ultra RNA Library Prep Kit for Illumina. Briefly, mRNA was purified from total RNA using poly-T oligo-attached magnetic beads. Fragmentation was carried out using divalent cations. First-strand cDNA was synthesized using random hexamer primers, followed by second-strand cDNA synthesis. After end repair and adapter ligation, the products were purified and enriched by PCR to create the final cDNA library.OrganizationMINSEQE ScoreAssays and DataMAGE-TAB FilesShuai LifalseTranscriptomic profiling of Guanxin Shuxin powder effects on a mouse model of coronary microvascular dysfunctionBiological 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.2026-06-11T00:00:00Z2026-06-11T01:00:46.717Z2026-06-01T14:09:30.816ZE-MTAB-17126ERP194189EFO_0002944EFO_0004170EFO_0005518EFO_0003738EFO_0004184