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Background Cardiac fibrosis following myocardial infarction (MI) drives adverse ventricular remodeling and heart failure, with cardiac fibroblasts (CFs) playing a central role

Targeted metabolomics analysis revealed that GGCT knockdown significantly reduced the abundance of TCA cycle intermediates, while GGCT overexpression substantially increased their levels

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PubChem CID: 44147413

DetectX Glutathione S-Transferase (GST) Fluorescent Activity Kit

Therefore, our finding highlights a novel aspect of STAT3/GIV pathway in the IL-17 promotes tumor angiogenesis of NSCLC.