Swiss researchers have gained new insights into the relationship between aging, inflammation, neurodegeneration and cognitive decline. EPFL professor Andrea Ablasser and her team showed that brain aging was driven by microglial activation of the cGAS/STING pathway.
A deficiency in fumarate metabolism could be behind a new mechanism of inflammation mediated by mitochondrial DNA and RNA. Two independent and simultaneous studies described how the accumulation of fumarate in the mitochondria released the genetic material of this organelle through vesicles, activating an inflammatory signaling pathway.
Researchers from The Salk Institute have described a signaling pathway that sets off an unusual, autophagy-dependent cell death mechanism as a fail-safe for cells that have evaded senescence mechanisms. The scientists found a tumor suppression mechanism mediated by telomere signaling, which activated an innate immune response through mitochondrial and telomere complexes to eliminate cells with shortened telomeres.
Following epigenetic STING (stimulator of interferon genes) derepression, inhibition of the MPS1 kinase strongly reactivated cGAS-STING signaling in mutations in both the oncogene KRAS and the tumor suppressor kinase LKB/STK11. Exploiting these findings could lead to a new therapeutic strategy to target treatment-refractory tumors with mutations in KL tumors, which have mutations in both KRAS and LKB1/STK11.
DUBLIN – After 18 months in stealth mode, Ventus Therapeutics Inc. has emerged with $60 million in series A funding and big ambitions to bring insights from structural biology to bear on two key aspects of innate immunity, inflammasome activation and cGAS-Sting signaling.