Chronic intermittent hypoxia triggers hepatic platelet recruitment

Obstructive sleep apnea (OSA) and its landmark feature intermittent hypoxia (IH), is increasingly recognized as an independent risk factor for liver disease occurrence and progression. Yet, the early molecular events linking IH to hepatic injury remain poorly understood. Using a murine model of chronic IH, we identified a platelet-related transcriptional response in the liver, marked by the upregulation of genes involved in platelet activation, aggregation, and neutrophil degranulation. In the rodent model, histological analyses confirmed intrahepatic platelet accumulation and neutrophil infiltration as early stage preceding overt fibrosis or steatosis. Liver biopsies from OSA patients revealed increased staining for activated platelets, supporting the translational relevance of our findings. Collectively, our data identify intrahepatic platelet recruitment and activation as early and conserved features of the hepatic response to IH, pointing to platelet-neutrophil interactions as potential contributors to OSA-associated liver injury.