ArticleJournal of molecular histology2026
Heparin-binding protein aggravates sepsis-induced acute lung injury by inhibiting the PERK-Nrf2-HO-1 signaling pathway.
Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Sepsis, a systemic inflammatory response disorder triggered by infection, often leads to multiple organ dysfunction syndrome. Sepsis-induced acute lung injury (SI-ALI) is among the most common complications. Heparin-binding protein (HBP), a major inflammatory mediator, has been demonstrated to induce vascular permeability and inflammation. Nevertheless, the mechanism by which HBP functions in sepsis-induced lung injury remains unclear. This study aimed to explore the role of HBP in sepsis-induced lung injury. A sepsis mouse model was established via cecal ligation and puncture (CLP), followed by HBP blockade using heparin. Serum inflammatory cytokine levels were measured by enzyme-linked immunosorbent assay (ELISA). Neutrophil infiltration was assessed by myeloperoxidase (MPO) activity. Lung tissue pathology was evaluated using hematoxylin-eosin (H&E) and Masson staining. Levels of ferrous iron (Fe
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