Michael P. Murphy

TL;DR: The description outlined here facilitates the understanding of factors that favour mitochondrial ROS production and develops better methods to measure mitochondrial O2•− and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.

TL;DR: In this article, a comparative in vivo metabolomic analysis was conducted to identify widely conserved metabolic pathways responsible for mitochondrial reactive oxygen species (ROS) production during ischaemia reperfusion.

TL;DR: It is demonstrated that upon lipopolysaccharide stimulation, macrophages shift from producing ATP by oxidative phosphorylation to glycolysis while also increasing succinate levels, and repurpose mitochondria from ATP synthesis to ROS production in order to promote a pro-inflammatory state.

TL;DR: It is shown that selective accumulation of the citric acid cycle intermediate succinate is a universal metabolic signature of ischaemia in a range of tissues and is responsible for mitochondrial ROS production during reperfusion, and a new pathway for metabolic control of ROS production in vivo is revealed.

TL;DR: In this article, mitochondria-targeted antioxidants have been developed by conjugating the lipophilic triphenylphosphonium cation to an antioxidant moiety, such as ubiquinol or α-tocopherol.