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Researchers described KPVs ability to modulate NF-B signaling and inflammatory cytokine expression independent of melanocortin receptor activation [1]

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The resulting downregulation of JMJD3 leads to suppressed EDNRB expression and compensatory upregulation of EDNRA, promoting endothelin-mediated vasoconstriction, ERK pathway activation, and vascular remodelingall key features of hypertension [55,56,57]

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That distinction is clinically meaningful