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We found that colistin leads to a rapid permeability transition of mitochondria isolated from mouse kidney that was fully prevented by co-incubation of the mitochondria with desensitizers of the mitochondrial transition pore cyclosporin A or L-carnitine

Exome sequencing reveals a de novo POLD1 mutation causing phenotypic variability in mandibular hypoplasia, deafness, progeroid features, and lipodystrophy syndrome (MDPL)

In vitro studies have elucidated a key mechanistic pathway underlying this effect: high concentrations of IL-6 and IL-1 excessively activate Ca 2+ channels on the erythrocyte membrane, leading to a pathological increase in intracellular Ca 2+ influx

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OH), and hydrogen peroxide (H 2 O 2 )