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Thirdly, inflammatory signaling: In myocardial infarction models, TMAO activates JAK2-STAT3 in cardiac fibroblasts, increasing JAK2/STAT3 phosphorylation and fibronectin/collagen I/III synthesis (Yang et al., 2025)

However, another report demonstrated mitochondrial stress and bioenergetics defects in GPx1 null mice ( Figure 3 ), and hence plays a key role in protecting phospholipids, cholesteryl esters and cardiolipin and defense against apoptosis and maintenance of ETC and OXPHOS ( + / - cells are sensitive to oxidative stress triggers (Muller et al., 2007)

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