Endothelial STING and STAT1 mediate IFN-independent effects of IL-6 in an endotoxemia-induced model of shock
Nina Martino; Erin Sanders; Ramon Bossardi Ramos; Iria Di John Portela; Fatma Awadalla; Shuhan Lu; Dareen Chuy; Neil Poddar · 2025 · Journal of Clinical Investigation
WASTE classifies this as Negative / Null Result Report · AI classification, approximate
The study found no significant effect — useful as a negative control or null benchmark for your own design.
Abstract
Severe systemic inflammatory reactions, including sepsis, often lead to shock, organ failure, and death, in part through an acute release of cytokines that promote vascular dysfunction. However, little is known about the vascular endothelial signaling pathways regulating the transcriptional profile in failing organs. Our work focused on signaling downstream of IL-6, due to its clinical importance as a biomarker for disease severity and predictor of mortality. Here, we show that loss of endothelial expression of the IL-6 pathway inhibitor SOCS3 promoted a type I IFN-like (IFNI-like) gene signat
Abstract by Nina Martino; Erin Sanders; Ramon Bossardi Ramos; Iria Di John Portela; Fatma Awadalla; Shuhan Lu; Dareen Chuy; Neil Poddar, Journal of Clinical Investigation (2025) — licensed CC BY 4.0.
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Metadata source: OpenAlex · DOI 10.1172/jci189570