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Open access Sep 2026

Intermedin mitigates chronic intermittent hypoxia-induced metabolic reprogramming in tubular epithelial cells and attenuates consequent kidney fibrosis through an AMPK-dependent suppression of HIF-1α.

It is demonstrated that IMD alleviates CIH-induced metabolic reprogramming in TECs and curbs kidney fibrosis via AMPK activation and consequent HIF-1α signaling, indicating that IMD suppresses HIF-1α through an AMPK-dependent mechanism.

Yuan Ge, Juan Pan, Ya-Nan Li et al. · 0 citations

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