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Highlights • HIF-1α and HIF-2α promote cellular adaptation to acute hypoxia, but during prolonged activation, these isoforms exert mutually antagonistic effects on the redox state and on proinflammatory pathways.• Imbalances… Click to show full abstract
Highlights • HIF-1α and HIF-2α promote cellular adaptation to acute hypoxia, but during prolonged activation, these isoforms exert mutually antagonistic effects on the redox state and on proinflammatory pathways.• Imbalances in HIF-1α and HIF-2α may contribute to the evolution and progression of chronic cardiac, vascular, and renal disorders.• Selective activation of HIF-2α can be achieved with drugs that inhibit isoform-selective PHDs or that promote the redox sensor, SIRT-1 (e.g., SGLT2 inhibitors).
Journal Title: JACC: Basic to Translational Science
Year Published: 2020
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