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In addition, GPX4 is highly expressed in most of acute myeloid leukemia (AML) subtypes compared to normal hematopoietic stem cells

One possible answer is that increased intracellular concentrations of either cation can lead to cellular hyperexcitability

What also concerned me was evidence that elevated TMAO compromises the release of nitric oxide release in endothelial cells thereby interfering with the vasodilatory mechanism which can contribute to hypertension

The vast majority of evidence comes from MCT or hypoxia animal models, whose pathological characteristics differ from human PH, lacking in-depth verification in models that are more similar to human disease states