James Eric Cox

This study shows that lactate can be directly imported into mitochondria and oxidized to support cardiac energy production, independent of the pyruvate carrier.

The paper identifies 9S-HODE, a lipid secreted by lean adipocytes, as a ferroptosis inducer that suppresses breast cancer while sparing normal cells, with therapeutic potential in obese mice.

This study shows that mitochondrial cardiolipin deficiency disrupts electron transport chain function, leading to oxidative stress and promoting MASH in mice and humans.

The paper describes a reversible form of suspended animation in C. elegans induced by high population density and identifies molecular mechanisms regulating its induction and termination.

This study identifies lipid metabolic reprogramming as a conserved mechanism conferring hypoxic and aging resilience in Arctic ground squirrels and C. elegans.

This study shows that N-acetylcarnosine treatment improves survival and delays age-related decline in multiple organ systems in female mice.

This study shows PGC-1α overexpression in skeletal muscle changes mitochondrial lipid composition but does not improve ATP synthesis efficiency.

This study shows that increased unsaturated fatty acids remodel the mitochondrial outer membrane by promoting the formation of mitochondrial-derived compartments and impairing TOM complex assembly.

This study shows semaglutide improves mitochondrial energy efficiency in skeletal muscle by enhancing ATP production per oxygen consumed during weight loss.

This study shows that heme biosynthesis regulates BCAA catabolism and thermogenesis in brown adipose tissue by affecting UCP1 and mitochondrial function.

This study shows that Schistosoma mansoni antigens induce innate immune training in males but not females, which can be inhibited by ovarian hormones and involves mitochondrial biogenesis.

This study identifies ZAG/AZGP1 as a secreted factor from triple-negative breast cancer cells that promotes fibrosis in the tumor microenvironment and is linked to poor patient prognosis.

This study uses isotope tracing to show that β-catenin mutations in HCC suppress phosphatidylcholine synthesis while increasing fatty acid oxidation.