Abstract
Hypoxia inducible factor-1 (HIF-1) is a transcription factor promoting many adaptive functions enhancing survival. HIF-1 is stabilized in hypoxia, whereas it rapidly degrades in normoxia via anti-oncogene Von Hippel Lindau (VHL) protein. We investigated acute rejection in recipients with HIF-1 deletion (no HIF-1 activity) or VHL deletion (constitutively stable HIF-1 activity) in myeloid cell lineage (granulocytes and monocyte/macrophages).
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