Michael P. Murphy

This study identifies TGS1 as a methyltransferase that modifies mRNAs encoding mitochondrial proteins in AML, promoting oxidative phosphorylation and cell survival, and shows its potential as a therapeutic target.

This study identifies CLN6 as a glycerophosphoglycerol epimerase essential for BMP biosynthesis, showing its deficiency disrupts lysosomal hydrolase homeostasis and can be reversed by BMP precursor supplementation.

This study identifies CLN8 as a stereospecific GPG acyltransferase critical for BMP biosynthesis, showing its loss causes Batten disease and that S,S-LPG supplementation can restore BMP and improve neurological symptoms.

This study measures mitochondrial oxygen affinity in carotid body and left ventricular tissue, finding slightly lower but not significantly different affinity in the carotid body, suggesting other factors, like NO, influence oxygen sensing.

The paper uses advanced imaging techniques to study mtDNA dynamics in quiescent human cells, revealing rapid replication and degradation rates and spatial organization of mtDNA.

In db/db mice, six weeks of AZD1656 improved diastolic function, cardiac metabolism and infarct size, with increased Treg infiltration and less fibrosis, without glycaemic change.

This study shows that COX4I2 in pericytes drives inflammation and emphysema in COPD by increasing mtROS, and its deletion protects against these effects.

This study develops an ovine model of maternal diet-induced obesity during pregnancy and finds fetal sex-specific changes in uterine vascular function.

This study evaluates optical brain pulse monitoring (OBPM) in a sheep model to detect middle cerebral artery occlusion and reperfusion by analyzing changes in brain pulse waveforms.

This study shows that an inherited mtDNA mutation alters inflammatory cytokine responses in macrophages and in vivo, leading to increased IFN-I and reduced pro-inflammatory cytokines.

This study shows that enhancing autophagy through redox regulation extends lifespan in Drosophila by highlighting the role of a specific cysteine residue in Atg4a.

The paper identifies mitochondrial reverse electron transport in myeloid cells as a driver of neuroinflammation and shows that blocking it protects the CNS in disease models.