Traumatic-hemorrhagic shock (T/HS) is a critical condition characterized by massive hemorrhage, hypovolemia, tissue hypoxia, and the progression to multi-organ dysfunction syndrome (MODS). To investigate the role of oxidized low-density lipoprotein receptor 1 (OLR1) in T/HS-induced liver injury, male Sprague-Dawley (SD) rats were utilized to establish a resuscitation after hemorrhagic shock (HS/R) model through controlled bloodletting and mean arterial pressure (MAP) monitoring. Immunohistochemical (IHC) staining revealed a significant upregulation of hepatic OLR1 expression following HS/R. Interfering with OLR1 significantly improved coagulation parameters, as evidenced by shortened thrombin time (TT), prothrombin time (PT), and activated partial thromboplastin time (APTT), along with reduced plasma thrombin-antithrombin (TAT) complex levels. Hematoxylin-eosin (HE) staining revealed extensive hepatocellular necrosis following HS/R, which was significantly alleviated by OLR1 knockdown. Biochemical analysis demonstrated reduced serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and pro-inflammatory cytokines (IL-1β and IL-18), highlighting the protective effect of OLR1 inhibition on liver function. Mechanistic studies revealed that OLR1 mediated HS/R-induced liver injury through the activation of the toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88) pathway and NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome- mediated pyroptosis, both of which were suppressed by OLR1 knockdown. These findings were corroborated in vitro using BRL-3A cells. In conclusion, OLR1 mediated HS/R-induced liver injury by regulating the TLR4/MyD88/NF-κB pathway and pyroptosis. Targeting OLR1 could offer a potential therapeutic strategy to mitigate liver damage, correct coagulation abnormalities, and improve outcomes in T/HS.