Hypoxia-induced hypercoagulability and thrombosis aggravation, which were reversed by transferrin knockdown and functional interference. (A-C) Effects of anti–Tf-AB, IgG control, RNR-Tf virus, blank (RNR) virus, HIF inhibitor LW6, or peptides TH16 and FX18 on APTT (A), PT (B), and bleeding time (C) in hypoxia-treated mice (n = 6-8). (D-E) Representative images of carotid artery blood flow (left) in FeCl₃-treated mice by laser speckle perfusion imaging (D), with region of interest (rectangle in white) placed in carotid artery to quantify blood flow change (E) (n = 6). Color bar at bottom indicates perfusion unit scale (0-989); scale bar represents 1 mm. Mice were subject to inferior vena cava (IVC) stenosis for 24 hours to evaluate venous thrombogenesis. (F-G) The pathological changes were observed through hematoxylin and eosin staining (F) and calculating thrombus weight (G) (n = 6-7); scale bar represents 200 μm. (H-I) Representative images of TTC-stained coronal brain sections (H) and quantitative analysis of stained area (I) on day 1 after tMCAO. Ischemic infarctions appear white, and brain infarct volumes were measured by planimetry (percentage of whole volume). (J-K) Bederson (J) and grip test (K) scores were also measured (n = 6-7); scale bar represents 0.5 cm. Animal experiments were repeated 3 times, independently. Data represent mean ± SD. Each point represents 1 mouse. Panels A-C, E, G, and I-K, ∗P < .05, ∗∗P < .01 by unpaired t test to compare; for example, Tf-AB and IgG groups or RNR-Tf and RNR groups.