Upregulation of HIF-1α in endothelial cells and myeloid-erived phagocytes (e.g., monocytes and macrophages) can also stimulate proinflammatory processes via mediators such as TNF-α, IL-1, and NO, leading to venous thrombosis.[35] In conclusion, the HIF pathway contributes to the regulation of physiological and pathological vessel wall remodeling (Fig. 7B). Here, HIF1A is linked to Venous thrombosis.