TNFa Downregulates STX17 Blocking Autophagy and Impairing Platelet Metabolism and Clot Contraction
Platelets are key players in hemostasis and thrombosis. In inflammatory conditions, platelets are hyperreactive and patients have an overal increased thrombotic risk. Our previous research demonstrated that TNFa significantly increases mitochondrial mass and platelet reactivity, emphasizing the crucial role of TNFa in modulating platelet metabolism and function.We hypothesized that TNFa disrupts platelet metabolism and function by inhibiting autophagy and mitophagy, which are critical processes for preserving mitochondrial mass, integrity, and energy production. We investigated the function, metabolism, and autophagy of human and mouse platelets in myeloproliferative neoplasms, rheumatoid arthritis, and aseptic inflammation. Our analysis reveled a blocked Overall design: RNA was extracted from platelets of three TNFdARE mice, and three control littermates. Bulk RNA sequencing was performed to determine transcriptional differences in platelets due inflammatory conditions mediated by TNFa