Andrew Phillip West

This study shows that tumor cell-intrinsic mtDNA instability drives temporal changes in the melanoma immune microenvironment through cGAS, affecting immune cell states and therapeutic response.

This study shows Coxiella burnetii uses its type IVB secretion system to suppress TLR3/TRIF signaling, inhibiting NF-κB and IRF responses during infection.

This study shows that the cGAS-STING pathway contributes to cancer-related fatigue in a mouse model of head and neck cancer, with STING inhibition reducing fatigue and inflammation.

This study shows that a 6-month lifestyle intervention reduces ER stress and inflammation while enhancing naive immune cell identity in older adults with metabolic disease.

This study shows that METTL14-dependent m6A modification prevents myocarditis and dilated cardiomyopathy by restraining IFN signaling and necroptosis in cardiomyocytes.

This study shows that genetic background and sex influence responses to intermittent fasting in mice, with effects on lifespan and health outcomes varying across strains.

This study identifies a shared genetic regulator linking metabolism and addiction-related behavior in mice and humans through a common enhancer regulating Eed/Me3 and EED/ME3.

This study shows that errors in mitochondrial translation cause cellular stress and metabolic changes linked to disease and aging, independent of oxidative phosphorylation.

This study shows that cGAS-STING-dependent type I IFN signaling is required for host defense against Leptospira interrogans in mice by reducing renal colonization.

This study identifies caspase-11 as a driver of macrophage hyperinflammation in Polg-related mitochondrial disease models, linking IFN-I signaling to exacerbated infection outcomes.

This study shows that mtDNA mutations in PolgD257A mice increase susceptibility to Mtb by impairing innate immunity and promoting necrosis.

This study uses optical metabolic imaging to identify metabolic shifts and mitochondrial heterogeneity in POLG mutator macrophages, revealing increased glycolytic dependence and subpopulation variability.

This study shows that aging reduces neuron growth potential in the CNS by impairing mitochondrial function in mice.

This study shows that GWIC exposure affects mitochondrial function and innate immune signaling in mice, leading to neurocognitive impairments and sex-specific differences.