HMGB1

[Journal of Clinical Investigation] The authors observed increased plasma and platelet surface expressed high mobility group box 1 in stroke patients. Mechanistically, platelets were identified as the critical source for HMGB1 causing neutrophil extracellular trap in the acute phase of stroke.

[Science Advances] Scientists demonstrated that the nuclear factor HMGB1 acts as a strong repressor of liver lipogenesis.

[Annals of Medicine] The authors comprehensively review the role of high-mobility group box 1 (HMGB1), hypoxia-inducible factor-1α (HIF-1α), and VEGF in doxorubicin-induced cardiovascular disease and its molecular mechanisms.

[Nature Communications] Pannexin-1 on endothelial cells acted as a conduit for ATP release that stimulated macrophage activation via P2X7 receptors and mitochondrial DNA release to increase IL-1β and HMGB1 secretion.

[Autophagy] Researchers identified ORF3a as an inducer of autophagy and revealed that ORF3a localized to the ER and induced RETREG1/FAM134B-related reticulophagy through the HMGB1-BECN1 pathway.

[Phytotherapy Research] Investigators explored the function of lucidone in tumor cytotoxicity and chemosensitivity through the suppression of receptor for advanced glycation end products-initiated signaling in pancreatic ductal adenocarcinoma cells.