Abstract
Macrophage is involved in hypertensive cardiovascular remodeling. We recently reported that inhibition of prolyl hydroxylase domain protein 2 (PHD2), which hydroxylates proline residue of hypoxia-inducible factor α (HIFα) and thereby induces HIFα degradation, suppressed inflammatory responses in macrophage. We examined whether myeloid-specific PHD2 deletion affects hypertension-induced cardiovascular remodeling.
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