Анна Степанова

Riding the tiger – physiological and pathological effects of superoxide and hydrogen peroxide generated in the mitochondrial matrix

Hydrogen peroxide as a central redox signaling molecule in physiological oxidative stress: Oxidative eustress

Hypoxia and intra-complex genetic suppressors rescue complex I mutants by a shared mechanism

Ferroptosis: molecular mechanisms and health implications

Use the Protonmotive Force: Mitochondrial Uncoupling and Reactive Oxygen Species

Maintenance of redox homeostasis by hypoxia-inducible factors

Mitochondrial composition and function under the control of hypoxia

Reactive oxygen species (ROS) as pleiotropic physiological signalling agents

Mitochondrial complex I deactivation is related to superoxide production in acute hypoxia

Hypoxia Rescues Frataxin Loss by Restoring Iron Sulfur Cluster Biogenesis

Structural basis for a complex I mutation that blocks pathological ROS production

Cellular adaptation to hypoxia through hypoxia inducible factors and beyond

Defining roles of specific reactive oxygen species (ROS) in cell biology and physiology

Ferroptosis as a Novel Therapeutic Target for Friedreich’s Ataxia

Complex I assembly into supercomplexes determines differential mitochondrial ROS production in neurons and astrocytes

Mitochondrial Respiratory Chain Complexes

Early VGLUT1-specific parallel fiber synaptic deficits and dysregulated cerebellar circuit in the KIKO mouse model of Friedreich ataxia

The Chemistry of Reactive Oxygen Species (ROS) Revisited: Outlining Their Role in Biological Macromolecules (DNA, Lipids and Proteins) and Induced Pathologies

Reactive Oxygen Species in Metabolic and Inflammatory Signaling

Ischemic A/D transition of mitochondrial complex I and its role in ROS generation

Effect of monovalent cations on the kinetics of hypoxic conformational change of mitochondrial complex I

Leigh Syndrome Mouse Model Can Be Rescued by Interventions that Normalize Brain Hyperoxia, but Not HIF Activation

Attenuation of oxidative damage by targeting mitochondrial complex I in neonatal hypoxic-ischemic brain injury

Early cerebellar deficits in mitochondrial biogenesis and respiratory chain complexes in the KIKO mouse model of Friedreich ataxia

The dependence of brain mitochondria reactive oxygen species production on oxygen level is linear, except when inhibited by antimycin A

Reverse electron transfer results in a loss of flavin from mitochondrial complex I: Potential mechanism for brain ischemia reperfusion injury