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Our findings, if validated in future studies with larger sample sizes, might suggest the potential for oxidative stress-targeted interventions to reduce thrombotic risk in thyroid dysfunction, as well as potential benefits from anti-thrombotic agents in severe thyroid disorders

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To further verify the mechanism, hepatocyte-specific DNA damage-inducible transcript 4 (DDIT4) knockout ( Ddit4 Hep ) mice were generated

Overall, PPAR effects stabilize metabolic homeostasis and preventor optimize responses tometabolic stress

Bottom row : Purinergic signaling, mediated by adenosine (A 1 , A 2A ) and P2-type (P2X 7 , P2Y 1 ) receptors, coordinates astrocytic inflammatory and metabolic responses