Next webinar on "Hypoxia & mitochondrial dynamics" will take place on 7th of November 2023 at 15:00 h CET

Our next webinar on “Hypoxia & mitochondrial dynamics” will take place on 7^th of November 2023 at 15:00 h CET and we are excited to announce the following speakers:

Control of bioenergetics and ROS from mitochondrial cristae

Rubén Quintana-Cabrera, PhD
Department of Molecular, Cellular and Developmental Neurobiology, Cajal Institute, CSIC, Madrid, Spain

My work aims to characterize the molecular determinants of mitochondrial physiology, particularly in the nervous system. Early during in my career at the University of Salamanca (Spain, lab Prof. Juan P. Bolaños) we described how γ-glutamylcysteine acts as a mitochondrial antioxidant in neuroprotective gene therapy. A research stage (EMBO STF, Univ. Geneva) expanded our results on the mitochondrial antioxidant capacity at the crossroads with mitochondrial dynamics and autophagy. I later contributed at the University of Padua (Italy, lab Prof. Luca Scorrano) to seminal works on how mitochondrial dynamics and ultrastructure set respiratory bioenergetics, tissue homeostasis and the sorting of mitochondria for autophagy, among others. We described how cristae engage ATPase oligomerization and activity to safeguard mitochondrial function. Back to the University of Salamanca with a Juan de la Cierva-Incorporación and Marie Curie-IF fellowships, I contributed to further works in neural metabolic and redox communication in the setting of neuroprotection and cognitive function. My current interests as a Ramón y Cajal principal investigator at the Cajal Institute (CSIC, Madrid) expand our studies on mitochondrial bioenergetics, redox, dynamics and metabolism to integrative responses during the acquisition of exogenous mitochondria and intercellular transfer, to uncover how mitochondrial content and functional reprogramming drive physio(patho)logy in the nervous system.


Na⁺ controls hypoxic redox signalling through the oxidative phosphorylation system

Pablo Hernansanz Agustín, PhD
Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain

All metazoans depend on the consumption of O₂ by the mitochondrial oxidative phosphorylation system (OXPHOS) to produce energy. In addition, the OXPHOS uses O₂ to produce reactive oxygen species (ROS) that can drive cell adaptations, a phenomenon that occurs during hypoxia. Ca²⁺ is the best-known ion that acts as a second messenger, yet the role ascribed to Na+ is to serve as a mere mediator of plasma membrane potential. Here we show that Na⁺ acts as a second messenger regulating OXPHOS function and the production of ROS by modulating the fluidity of the inner mitochondrial membrane (IMM). A conformational shift in mitochondrial complex I during acute hypoxia drives acidification of the matrix and the release of free Ca²⁺ from calcium phosphate precipitates. The concomitant activation of the mitochondrial Na⁺/Ca²⁺ exchanger (NCLX) promotes the import of Na⁺ into the matrix. Na⁺ interacts with phospholipids, reducing IMM fluidity and the mobility of free ubiquinone between complex II and complex III, but not inside supercomplexes. As a consequence, superoxide is produced at complex III. The inhibition of Na⁺ import through NCLX is sufficient to block this pathway, preventing adaptation to hypoxia. These results reveal that Na+ controls OXPHOS function and redox signalling through an unexpected interaction with phospholipids, with profound consequences for cellular metabolism.

How can I join the webinar?

https://us06web.zoom.us/j/86469731540?pwd=Mu9W9zBMm65TpJb6k4pwviFjseHQxw.OgbiZAvSiHJI7kVt

Passcode: 433382

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the SFRR-E ECR subcommittee