Sonia Mercurio

TL;DR: This review focuses on recent findings highlighting the importance of controlling intracellular heme levels to counteract heme-induced oxidative stress and the involvement of genes orchestrating heme metabolism in several pathological conditions.

TL;DR: Feline leukemia virus subgroup C receptor 1 regulates erythropoiesis by controlling mitochondrial heme efflux, whereas FLVCR1a expression is required to prevent hemorrhages and edema, and the aberrant expression of Flvcr1 isoforms may play a role in the pathogenesis of disorders characterized by an imbalance between heme and globin synthesis.

TL;DR: The regulatory role of heme during erythroid differentiation is discussed as well as the heme-mediated regulatory mechanisms that allow the orchestration of the adaptive cell response to heme deficiency.

TL;DR: In livers of mice, Flvcr1a maintains a free heme pool that regulates heme synthesis and degradation as well as cytochromes P450 expression and activity, which has important implications for drug metabolism.

TL;DR: Consistently, reduction or increase of the cytosolic heme rescued the erythroid defects in zebrafish deficient in Flvcr1a or FlvCr1b, respectively, suggesting heme export represents a tightly regulated process that controls erythropoiesis.