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Oxana Kunduzova

Researcher at French Institute of Health and Medical Research

Publications -  8
Citations -  836

Oxana Kunduzova is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: Oxidative stress & Kidney. The author has an hindex of 7, co-authored 8 publications receiving 783 citations. Previous affiliations of Oxana Kunduzova include Paul Sabatier University.

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Oxidative Stress by Monoamine Oxidase Mediates Receptor-Independent Cardiomyocyte Apoptosis by Serotonin and Postischemic Myocardial Injury

TL;DR: The results supply the first direct evidence that oxidative stress induced by MAO is responsible for receptor-independent apoptotic effects of 5-HT in cardiomyocytes and postischemic myocardial injury.
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Oxidative Stress–Dependent Sphingosine Kinase-1 Inhibition Mediates Monoamine Oxidase A–Associated Cardiac Cell Apoptosis

TL;DR: It is shown for the first time that the upregulation of ceramide/sphingosine 1-phosphate ratio is a critical event in MAO-A–mediated cardiac cell apoptosis and the first evidence linking generation of reactive oxygen species with SphK1 inhibition is provided.
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Apelin, a promising target for type 2 diabetes treatment?

TL;DR: This review describes the various metabolic functions that are affected by apelin and presents an integrated overview of recent findings that collectively propose apelin as a promising target for the treatment of T2DM.
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Regulation of JNK/ERK activation, cell apoptosis, and tissue regeneration by monoamine oxidases after renal ischemia-reperfusion.

TL;DR: The crucial role of MAOs in mediating the production of injurious ROS, which contribute to acute apoptotic and necrotic cell death induced by renal ischemia‐reperfusion in vivo, is demonstrated.
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Prevention of apoptotic and necrotic cell death, caspase-3 activation, and renal dysfunction by melatonin after ischemia/reperfusion

TL;DR: The demonstration that melatonin prevents postreperfusion apoptotic and necrotic cell death and improves renal function suggests thatMelatonin may represent a novel therapeutic approach for prevention of I/R injury.