Loss of stimulator of interferon genes (STING) promotes accumulation of cholesterol and triglycerides throughout life in mice

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dc.article.number45
dc.catalogadorpau
dc.contributor.authorRiquelme, Ian
dc.contributor.authorCarrillanca, Daniela
dc.contributor.authorSánchez-Pérez, Camila
dc.contributor.authorMonterroza, Andrea
dc.contributor.authorHernández-Rojas, Bairon
dc.contributor.authorRiadi, Gonzalo
dc.contributor.authorCancino Lobos, Gonzalo Ignacio
dc.contributor.authorMurgas, Paola
dc.date.accessioned2025-07-08T20:01:45Z
dc.date.available2025-07-08T20:01:45Z
dc.date.issued2025
dc.date.updated2025-07-06T00:06:29Z
dc.description.abstractAbstract Background The Stimulator of Interferon Genes (STING) pathway is pivotal in innate immunity, facilitating the detection of cytosolic DNA and initiating type I interferon-dependent responses. In addition to its immunological roles, STING has been increasingly associated with metabolic regulation, since research indicates that its inhibition can diminish inflammation, lipid accumulation, and tissue damage in obesity and other metabolic disorders. The findings have prompted the suggestion of STING inhibition as a viable treatment approach for metabolic illness. Nonetheless, the physiological function of STING in lipid homeostasis under normal settings remains largely unexplored, as does the impact of its absence on metabolism throughout various life stages in the absence of disease. This information deficit is crucial, particularly in light of the increasing interest in the long-term pharmacological suppression of STING. Results To examine the function of STING in lipid metabolism during physiological, non-pathological conditions throughout the lifespan, we assessed WT and STINGKO mice at various ages and discovered that STING deficiency results in a consistent increase in body weight, independent of alterations in locomotor activity or food consumption. STINGKO mice exhibited markedly increased circulation levels of triglycerides and total cholesterol. Histological and morphological analysis demonstrated augmented fat accumulation in adipose and hepatic tissues, despite the lack of nutritional or genetic metabolic stress. These findings indicate a crucial function for STING in the control of lipid homeostasis across the lifespan. Conclusions In contrast to earlier research conducted under pathological conditions, our findings indicate that the total absence of STING expression in healthy contexts leads to heightened lipid accumulation in tissues and blood. These findings underscore an unforeseen function of STING as a modulator of lipid metabolism in the context of longevity. They caution against the prolonged use of STING inhibitors, as chronic STING suppression may lead to detrimental metabolic effects. This study offers new insights into the non-immune roles of STING, indicating its significance in preserving metabolic equilibrium throughout the lifetime.
dc.fechaingreso.objetodigital2025-07-08
dc.format.extent17 páginas
dc.identifier.citationBiological Research. 2025 Jul 02;58(1):45
dc.identifier.urihttps://doi.org/10.1186/s40659-025-00624-3
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/104879
dc.information.autorucFacultad de Ciencias Biológicas; Cancino Lobos, Gonzalo Ignacio; S/I; 17709
dc.issue.numero58
dc.nota.accesocontenido completo
dc.revistaBiological Research
dc.rightsacceso abierto
dc.rights.holderThe Author(s)
dc.subjectSTING
dc.subjectLipid metabolism
dc.subjectTriglycerides
dc.subjectCholesterol
dc.subjectAging
dc.subjectAdipose tissue
dc.subjectHepatic steatosis
dc.subjectMetabolic control
dc.subjectInnate immunity
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleLoss of stimulator of interferon genes (STING) promotes accumulation of cholesterol and triglycerides throughout life in mice
dc.typeartículo
sipa.codpersvinculados17709
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