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Marinobufagenin is an endogenous bufadienolide steroid, originally isolated from toad venom but present in humans as well. It is a potent inhibitor of sodium-potassium ATPase and acts mainly on the α1 isoform in renal and vascular tissue. By altering ionic gradients and signaling, it induces natriuresis, vasoconstriction, and positive inotropic effects, while also promoting cardiac and vascular fibrosis via distinct signaling pathways. MBG concentrations are elevated in a variety of cardiovascular and renal pathologies—including heart failure, chronic kidney disease, pre-eclampsia, and essential hypertension—and are considered both potential biomarkers and therapeutic targets in these conditions. Mineralocorticoid receptor antagonists can block MBG-induced fibrosis. MBG also influences inflammation, immune cell function, and may have roles in cancer and neurological processes. Safety concerns include its cardiotoxicity and contribution to organ fibrosis when present at elevated levels[2][4][5][7][8].
Inhibition of Na^+/K^+-ATPase leading to altered ionic homeostasis, natriuresis, and vasoconstriction; Activation of intracellular signaling (MAPK, ROS); Fibrosis via inhibition of Fli1 transcription factor (and modification of collagen synthesis); Modulation of immune signaling; Modulation of mineralocorticoid receptor transcriptional activity (interference rather than activation)
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