Daniel Barnett

Keywords reactive oxygen species mitochondria electron leak cell metabolism cell signaling pathways complex I complex III disease mechanisms Get full text access Log in, subscribe or purchase for full access. References 1. Andersson, S.G. ∙ Kurland, C.G. Origins of mitochondria and hydrogenosomes Curr. Opin. Microbiol. 1999; 2:535-541 2. Brand, M.D. Riding the tiger - physiological and pathological effects of superoxide and hydrogen peroxide generated in the mitochondrial matrix Crit. Rev. Biochem. Mol.

Abstract Current whole-genome spatial transcriptomics (ST) platforms, which range from multicellular (e.g., Visium) to subcellular resolution (e.g., Visium HD, Stereo-seq), face significant challenges in accurately decomposing or aggregating spots into single cells—the fundamental units of biological activity. To date, most existing computational methods operate at the spot level, and no method has effectively reconstructed transcriptomes at single-cell resolution.

Abstract Neurodegenerative disorders alter mitochondrial functions, including the production of reactive oxygen species (ROS). Mitochondrial complex III (CIII) generates ROS implicated in redox signalling, but its triggers, temporal dynamics, targets and disease relevance are not clear.