Zanou Nadege

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BEC 2020.1 Mitochondrial physiology
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COST Action CA15203 (2016-2021): MitoEAGLE
Evolution-Age-Gender-Lifestyle-Environment: mitochondrial fitness mapping

Zanou Nadege

MitoPedia topics: EAGLE 

COST: Member COST WG1: WG1


Name Zanou Nadege, PhD
Institution Department of Physiology

Institute of Sport Sciences

Faculty of Medicine and Biology

UniversitΓ© de Lausanne, CH

Address ,
City Lausanne
Country Switzerland
Email [email protected]
O2k-Network Lab CH Lausanne Place N

Labels: Field of research: Basic 


Donnelly 2024 Redox Biol2024Donnelly C, KomlΓ³di T, Cecatto C, Cardoso LHD, Compagnion A-C, Matera A, Tavernari D, Campiche O, Paolicelli RC, Zanou N, Kayser B, Gnaiger E, Place N (2024) Functional hypoxia reduces mitochondrial calcium uptake. Redox Biol 71:103037.
Zanou 2021 Nat Commun2021Zanou N, Dridi H, Reiken S, Imamura de Lima T, Donnelly C, De Marchi U, Ferrini M, Vidal J, Sittenfeld L, Feige JN, Garcia-Roves PM, Lopez-Mejia IC, Marks AR, Auwerx J, Kayser B, Place N (2021) Acute RyR1 Ca2+ leak enhances NADH-linked mitochondrial respiratory capacity. Nat Commun 12:7219.
BEC 2020.1 doi10.26124bec2020-0001.v12020Gnaiger E et al ― MitoEAGLE Task Group (2020) Mitochondrial physiology. Bioenerg Commun 2020.1.


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MitoEAGLE Short-Term Scientific Mission

Motivation letter
I am medical doctor with a Ph.D in skeletal muscle physiology and pathophysiology obtained in Brussels, Belgium in 2012. I was postdoctoral researcher for the National Scientific Research Foundation of Belgium from 2013 to 2015 and first assistant at the University of Lausanne since November 2015 for a 5-year contract.
My areas of expertise are skeletal muscle biology, contraction and mechanical measurement, development and regeneration, calcium signalling pathways and muscular dystrophy.
I am currently working on the molecular mechanisms of skeletal muscle adaptations to the high intensity interval training (HIIT) and the role of the ryanodine receptor type 1 (RyR1) in the process. Indeed, in a previous work (Place et al, PNAS 2015), our group showed some structural modifications of RyR1 in response to HIIT. We then aimed at investigating the nature of these RyR1 modifications in response to HIIT and their effects on muscle plasticity and mitochondrial biogenesis in different models. I already set up a model of electrical stimulation of myotubes mimicking HIIT. We planned to combine this with other models such as isolated whole mouse muscle or single muscle fibres submitted to a HIIT-mimicking electrical stimulation and muscles from mice or humans performing HIIT exercise, to tackle the question of HIIT-induced RyR1 modifications and their role in muscle plasticity and metabolism. We have just submitted a grant proposal to our national funding agency and our plan is to use a translational approach (from myotubes to patients) to gain insights into the mechanisms underlying muscle remodelling after acute or chronic HIIT.
The ultimate goal of our present approach is to unpack the role of RyR1 changes for the stimulation of mitochondrial biogenesis upon HIIT. However, I have limited experience in the muscle metabolism field, reason why we contact the MitoEagle to extend my arsenal of skills.
Interestingly, Professsor Garcia-Roves from the University of Barcelona has recently developed a high-resolution respirometry for mitochondrial characterization ex vivo, which constitutes a very exciting tool for us. I already obtained his agreement to spend 3 weeks in his lab early 2017 in the context of MitoEAGLE scientific mission (see attached his letter of agreement).
STSM request: download pdf
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