Integrated metabolomic profiling reveals metabolomic responses by epicardial and myocardial stromal cells to ischemia.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Cardiac ischemia induces substantial metabolomic reprogramming, which dysregulates cardiomyocytes (CMs) and non-myocyte stromal cell populations. The stromal cells derived from epicardial adipose tissue (EAT) and ventricle are critical for extracellular matrix (ECM) remodeling, paracrine signaling, and myocardial homeostasis. However, the metabolomic content and responses of EAT-derived stromal cells (EATDS) and ventricular stromal cells (VSCs) remain unknown. This study employed untargeted liquid chromatography-mass spectrometry (LC-MS)-based metabolomics to characterize ischemia-driven metabolic reprogramming in EATDS and VSCs harvested from swine hearts. Ischemia was simulated using the standard ischemic buffer (pH 6.2) for 2 h. Metabolomic screening revealed 65 and 68 metabolites, respectively, for EATDS and VSCs. Results revealed extensive downregulation of amino acid biosynthesis, redox pathways, and mitochondrial metabolism, alongside selective upregulation of glycolytic and cofactor-associated metabolites. Pathway enrichment analyses indicated significant suppression of the TCA cycle, one-carbon metabolism, glutathione cycling, and branched-chain amino acid degradation, reflecting impaired bioenergetic and antioxidant capacity. Adaptive responses included the enrichment of glycolysis, β-alanine, and glyoxylate/dicarboxylate metabolism, consistent with metabolic plastici

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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