P. S. Brookes

Reactive Oxygen Species Generation by Reverse Electron Transfer at Mitochondrial Complex I Under Simulated Early Reperfusion Conditions.

The paper investigates ROS generation during reperfusion, finding that Cx-I RET contributes less than previously thought, with other sources contributing significantly.

A kidney-hypothalamus axis promotes compensatory glucose production in response to glycosuria

This study shows that afferent renal nerves promote compensatory glucose production in response to glycosuria by activating the hypothalamic-pituitary-adrenal axis in mice.

Distinct effects of intracellular vs. extracellular acidic pH on the cardiac metabolome during ischemia and reperfusion.

This study investigates how intracellular and extracellular acidic pH affect cardiac metabolism during ischemia and reperfusion, finding distinct metabolic changes induced by each condition.

Inhibiting succinate release worsens cardiac reperfusion injury by enhancing mitochondrial reactive oxygen species generation

This study shows that inhibiting succinate release during reperfusion increases mitochondrial ROS and worsens cardiac injury by promoting PT pore opening.

Metabolomics of aging in primary fibroblasts from small and large breed dogs

This study uses metabolomics to compare aging patterns in small and large breed dogs, finding size-specific metabolic changes linked to lifespan differences.

Complex effects of pH on ROS from mitochondrial complex II driven complex I reverse electron transport challenge its role in tissue reperfusion injury

The paper investigates how pH affects ROS production via mitochondrial complex II to complex I reverse electron transport during reperfusion injury and finds that ROS generation is insensitive to pH despite changes in mitochondrial respiration.

ALKBH7 mediates necrosis via rewiring of glyoxal metabolism

This study shows ALKBH7 regulates glyoxal metabolism, and its deficiency protects against necrosis and ischemia-reperfusion injury through hormetic signaling involving methylglyoxal stress.

Cardioprotection by the mitochondrial unfolded protein response (UPRmt) is mediated by activating transcription factor 5 (ATF5)

This study shows that ATF5 is required for cardioprotection induced by UPRmt activators against ischemia-reperfusion injury.

Cardioprotection by nicotinamide mononucleotide (NMN): Involvement of glycolysis and acidic pH.

This study shows NMN protects hearts from ischemia-reperfusion injury by stimulating glycolysis and acidosis, with protection independent of SIRT1.

Cardiac metabolic effects of KNa1.2 channel deletion, and evidence for its mitochondrial localization.

This study identifies a cardiac mitochondrial KNa1.2 channel and shows its role in regulating metabolism during high energetic demand.