Leon Kiriaev
Leon Kiriaev
Dr Leon Kiriaev is a Research Officer in the Muscle Research Group at the Murdoch Children's Research Institute. In 2022 he obtained his PhD from the faculty of medicine at Western Sydney University/UNSW where he investigated the role of branched skeletal muscle fibres in the pathogenesis of Duchenne Muscular Dystrophy and the influence of ACTN3 deficiency as a genetic modifier.
Incorporating contractile physiology, imaging and molecular biology techniques, he has helped investigate various genetic mutations that impact muscle performance (ACTN3, PYROXD1, NMNAT1, Duchenne, dysferlinopathy) and explore the effects of treatment strategies (NAC, minocycline, notexin, ASO therapies, DHT) to help understand and develop therapeutic targets for neuromuscular diseases.
Currently, his research focus is on modelling neuromuscular diseases to investigate therapeutic strategies and the effects of ACTN3 R577X deficiency on glycogen metabolism and metabolic health.
Incorporating contractile physiology, imaging and molecular biology techniques, he has helped investigate various genetic mutations that impact muscle performance (ACTN3, PYROXD1, NMNAT1, Duchenne, dysferlinopathy) and explore the effects of treatment strategies (NAC, minocycline, notexin, ASO therapies, DHT) to help understand and develop therapeutic targets for neuromuscular diseases.
Currently, his research focus is on modelling neuromuscular diseases to investigate therapeutic strategies and the effects of ACTN3 R577X deficiency on glycogen metabolism and metabolic health.
Dr Leon Kiriaev is a Research Officer in the Muscle Research Group at the Murdoch Children's Research Institute. In 2022 he obtained his PhD from the faculty of medicine at Western Sydney University/UNSW where he investigated the role of branched...
Dr Leon Kiriaev is a Research Officer in the Muscle Research Group at the Murdoch Children's Research Institute. In 2022 he obtained his PhD from the faculty of medicine at Western Sydney University/UNSW where he investigated the role of branched skeletal muscle fibres in the pathogenesis of Duchenne Muscular Dystrophy and the influence of ACTN3 deficiency as a genetic modifier.
Incorporating contractile physiology, imaging and molecular biology techniques, he has helped investigate various genetic mutations that impact muscle performance (ACTN3, PYROXD1, NMNAT1, Duchenne, dysferlinopathy) and explore the effects of treatment strategies (NAC, minocycline, notexin, ASO therapies, DHT) to help understand and develop therapeutic targets for neuromuscular diseases.
Currently, his research focus is on modelling neuromuscular diseases to investigate therapeutic strategies and the effects of ACTN3 R577X deficiency on glycogen metabolism and metabolic health.
Incorporating contractile physiology, imaging and molecular biology techniques, he has helped investigate various genetic mutations that impact muscle performance (ACTN3, PYROXD1, NMNAT1, Duchenne, dysferlinopathy) and explore the effects of treatment strategies (NAC, minocycline, notexin, ASO therapies, DHT) to help understand and develop therapeutic targets for neuromuscular diseases.
Currently, his research focus is on modelling neuromuscular diseases to investigate therapeutic strategies and the effects of ACTN3 R577X deficiency on glycogen metabolism and metabolic health.
Top Publications
- Kiriaev, L, Baumann, CW, Lindsay, A. Eccentric contraction-induced strength loss in dystrophin-deficient muscle: Preparations, protocols, and mechanisms.. J Gen Physiol 155(2) : 2023 view publication
- Redwan, A, Kiriaev, L, Kueh, S, Morley, JW, Houweling, P, Perry, BD, Head, SI. Six weeks of N-acetylcysteine antioxidant in drinking water decreases pathological fiber branching in MDX mouse dystrophic fast-twitch skeletal muscle.. Front Physiol 14: 1109587 2023 view publication
- Haug, M, Reischl, B, Nübler, S, Kiriaev, L, Mázala, DAG, Houweling, PJ, North, KN, Friedrich, O, Head, SI. Absence of the Z-disc protein α-actinin-3 impairs the mechanical stability of Actn3KO mouse fast-twitch muscle fibres without altering their contractile properties or twitch kinetics.. Skelet Muscle 12(1) : 14 2022 view publication
- Kiriaev, L, Houweling, PJ, North, KN, Head, SI. Loss of α-actinin-3 confers protection from eccentric contraction damage in fast-twitch EDL muscles from aged mdx dystrophic mice by reducing pathological fibre branching.. Hum Mol Genet 31(9) : 1417 -1429 2022 view publication
- Kiriaev, L, Kueh, S, Morley, JW, Houweling, PJ, Chan, S, North, KN, Head, SI. Dystrophin-negative slow-twitch soleus muscles are not susceptible to eccentric contraction induced injury over the lifespan of the mdx mouse.. Am J Physiol Cell Physiol 321(4) : C704 -C720 2021 view publication
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