Montserrat Vega is a postdoctoral researcher at Pompeu Fabra University (Spain). In 2016 she obtained a double PhD in Functional and Molecular Biology from the University of Oviedo (Prof. Fernando Moreno lab) and the University of Osnabrück (Prof. Jürgen Heinisch lab) studying glucose transcriptional response in Saccharomyces cerevisiae. In 2017 Montserrat joined the laboratory of Elena Hidalgo at Pompeu Fabra University. She is interested in studying the molecular mechanism that control aging in Schizosaccharomyces pombe, specifically in uncovering the connection between mitochondrial function, aging and how a deregulation of the different mechanisms in charge of controlling mitochondrial homeostasis could alter lifespan.

This information was published in June 2024, if you need updated information, please contact the award winner.

Aging is characterized by a general decline in cellular functions that leads to higher risk of disease and finally to death. Health span is affected not only by the environment, but it is also determined by genetic traits and by molecular pathways. There is a strong correlation between aging and cellular metabolism, proved by the fact that calorie restriction extends lifespan of different species. The main metabolic pathway for energy production is oxidative phosphorylation that takes place within the mitochondria. Cells can sense glucose levels and finetune ATP production accordingly. Regulation of the respiratory capacity can take place at different levels: transcriptomic, proteomic, or regulation of mitochondrial activity. Regarding the last, one of the mechanisms that has been recently described to increase respiratory efficiency is the arrangement of individual respiratory complexes into major structures called supercomplexes (SCs). Although some aspects of their functional organization remain still under study, it has been proposed that SCs maximize the electron flux and decrease ROS production. By using the yeast Schizossacharomyces pombe, this proposal aims at: (i) identifying key factors involved in the functional composition of SCs and (ii) studying their possible function in respiratory efficiency, ROS production and connection with the aging process.

Timoteo Marchini is the Deputy Lab Head of the Vascular Immunology Laboratory (PI: Prof. Dr. Dennis Wolf) at the Department of Cardiology and Angiology of the University Medical Center Freiburg (Germany). After obtaining his Biochemistry degree at the University of Buenos Aires (Argentina), he conducted his MSc and PhD studies on redox and mitochondrial mechanisms leading to impaired cardiac contractility in mice exposed to air pollution particles (PM2.5). During his first postdoctoral training at the “Instituto de Bioquímica y Medicina Molecular Prof. Alberto Boveris (IBIMOL-UBA-CONICET)”, Timoteo studied inflammatory pathways in ischemia/reperfusion injury and myocardial remodelling in mice exposed to polluted urban air. Currently, his research focuses on redox and immune mechanisms linking air pollution PM2.5 exposure and the accelerated development of risk factors for cardiovascular disease, such as obesity. Timoteo has received several international awards, including the 2019 YIA (OCC), the 2021 YIA (SFRR-E), and the 2022 Future of Redox Award (SFRR-I). He has also been actively involved in outreach activities, including the publication of several scientific communication articles and book chapters related to his research.

This information was published in June 2024, if you need updated information, please contact the award winner.

In Europe, air pollution causes ~790,000 premature deaths per year, with nearly half linked to cardiovascular diseases (CVD). Notably, it has been increasingly highlighted that the development of risk factors for CVD (e.g., hypertension, obesity, and diabetes) partially explains the negative health impact of air pollution on CVD incidence and mortality. Among a complex mixture of several toxic chemical compounds, airborne particles smaller than 2.5 μm (PM2.5) are the most hazardous air pollutant. PM2.5 exposure impairs pulmonary redox metabolism and inflammation, orchestrated by lung resident immune cells known as alveolar macrophages. This promotes a systemic response that alters function in distant organs, including the blood vessels, the heart, and adipose tissue. However, the interaction between immune cells and

adipocytes leading to PM2.5-induced metabolic derangements that are associated with aggravated CVD is poorly understood. This project aims to unravel cell-specific effects of PM2.5 in adipose tissue, with particular focus on the mechanistic link between altered redox metabolism and inflammatory pathways. The present research will highlight the contribution of environmental factors in the development of risk factors for CVD and, ultimately, will build the conceptual basis to design interventional strategies in the future, as well as to increase awareness within the general population.

Valeria Cordone graduated in Biotechnologies at the University of L’Aquila (Italy), and achieved the Ph.D. in Cellular and Molecular Biotechnologies (2019). Since 2019 she has been a post-doc fellow at the University of Ferrara. In 2020, she won a prestigious Post Doctoral Fellowship, founded by Umberto Veronesi Foundation and ProRETT Onlus, presenting a project entitled ‘Role of inflammasome in Rett Syndrome’. Her research mainly focuses on investigating molecular and cellular mechanisms related to the synergistic condition of oxidative stress and chronic subclinical inflammation (“OxInflammation”), involved in the pathogenesis of neurodevelopmental disorders, like Rett Syndrome. These studies involve the analysis of pathways upstream and downstream of the inflammasome activation, as well as the interaction between Nrf2 and NF-κB, in mediating the OxInflammatory damage and participating in the multi-systemic alterations characterizing the aforementioned pathology.

This information was published in June 2024, if you need updated information, please contact the award winner.

Rett syndrome (RTT) is a severe neurodevelopmental disorder with a genetic cause (i.e., loss-of-function mutations of MECP2 gene). Beside the neurological aspects, RTT patients show a multitude of co-morbidities, affecting other organs and tissues, as well as impaired cellular/molecular signalling pathways, including mitochondrial dysfunctions, oxidative stress, and an altered immune-inflammatory status, acting in a vicious circle defined as ‘OxInflammation’. A constitutive activation of NLRP3 inflammasome system, which is a multi-protein complex involved in innate immune responses against both pathogens and ROS-related cellular stress, has recently been shown to play a critical role in the sub-clinical inflammation typical of this pathology.

In light of this, the proposed project aims at investigating whether an excess of reactive oxygen species or an impairment of mitophagy (a crucial process where damaged mitochondria are delivered to lysosomes for their removal) may be involved in the continuous stimulation of NLRP3 inflammasome system, occurring in RTT condition. The results of this project will help to elucidate new molecular mechanisms underlying this complex pathology.

Nikos Margaritelis is an Assistant Professor of Research Methods and Data Analysis at the Department of Physical Education and Sports Science of the Aristotle University of Thessaloniki, Greece. During his PhD, his work focused on the redox inter-individual variability and its implications on differential physiological and biochemical responses and adaptations after exercise. Over the past years, he aimed to investigate the potential need for personalized interventions based on the observed redox heterogeneity among individuals, exemplified by subject-tailored antioxidant supplementation schemes. To this aim, he designed and implemented methodological designs and analyses in order to contribute to a nuanced understanding of redox personalization. In addition to his primary focus, his research interests also include: (i) the practicality of the erythrocyte as a ‘model’ for studying the intersection of redox biology and physiology; (ii) the translational potential of oxidative stress biomarkers; and (iii) the epistemological foundations of the oxidative stress concept.

This information was published in June 2024, if you need updated information, please contact the award winner.

Personalized treatments are considered the scientific breakthrough that will revolutionize healthcare systems and promote well-being. At the same time, redox biology processes are increasingly recognized an essential part of health and disease.

Clinical trials using redox agents yielded conflicting results, which stressed the potential need for personalized strategies. Currently, personalized treatments remain more of a buzzword instead of a routine practice. The RedoxOne project is a translational redox-oriented version of personalization, built upon the idea that even the fundamental prerequisites of personalized treatments have not been confirmed, which could partially explain the ‘failure’ of the personalized concept. Specifically, personalization presupposes that (i) large interindividual redox variability exists; (ii) this variability is biologically meaningful; (iii) the response of each individual is truly unique. RedoxOne aspires to unravel these issues by conceptualizing and exploiting a novel methodological approach, the N-of-1 trials. This demands the synthesis of several fields, which for the needs of the project are redox biology, metabolism, research methods, statistics and exercise physiology. RedoxOne will add scientific and translational potential to deliver a unifying theory for personalized interventions. Are humans really redox unique? Or more elegantly, are we as diverse as we think we are, to necessitate personalized redox treatments?

Dr. Sophie Hendrix is a postdoctoral researcher at Hasselt University (Belgium). She investigates plant responses to abiotic stress factors with a strong focus on redox processes. During her PhD at Hasselt University, she studied the effects of cadmium stress on cell cycle regulation and the DNA damage response in Arabidopsis. Afterwards, she worked as a Humboldt postdoctoral fellow at the University of Bonn (Germany), where she investigated plant responses to heat stress using genetically encoded biosensors and studied the role of plant glutathione peroxidase-like proteins. Her current work focuses on unravelling the involvement of the SOG1 transcription factor in oxidative signalling in plants.

This information was published in 2023, if you need updated information, please contact the award winner.

Cadmium (Cd) pollution is a significant environmental concern and Cd uptake in plants poses a major threat to global food security. Hence, it is crucial to increase our knowledge on plant responses to Cd stress. My PhD research revealed that the transcription factor suppressor of gamma response 1 (SOG1) contributes to Cd-induced cell cycle inhibition in Arabidopsis thaliana. Furthermore, I identified a novel role for SOG1 in Cd-induced oxidative signalling. The sog1-7 knockout mutant displayed an enhanced tolerance to short-term Cd exposure, which coincided with delayed Cd-induced reactive oxygen species (ROS) production and transcriptional activation of ethylene biosynthesis and signalling. However, the larger extent of lipid peroxidation in this genotype upon prolonged Cd exposure suggests that the lack of appropriate oxidative signalling results in sub-optimal stress acclimation. In the proposed project, I aim to further characterize this newly identified role of SOG1 and identify the SOG1 downstream targets mediating Cd-induced oxidative signalling via a combination of genetic, molecular and biochemical approaches. Furthermore, I will investigate whether SOG1 also mediates oxidative signal transduction upon exposure to salinity, heat and methyl viologen to reveal whether this transcription factor plays a conserved role in plant responses to ROS-inducing stress condition.

Dr. Verónica Miguel is a postdoctoral researcher in the immunobiology laboratory at the Spanish National Centre for Cardiovascular Research (Dr. David Sancho´s lab). She completed her PhD at the Center for Molecular Biology "Severo Ochoa” in Spain (Dr. Santiago Lamas´ lab), receiving the Extraordinary PhD Award from the Autonomous University of Madrid. She has been dedicated to investigate the metabolic alterations underlying chronic kidney disease, demonstrating that the enhancement of fatty acid oxidation protects against the development of renal fibrosis. She also identified new miRNAs involved in renal fibrosis directly related with the regulation of redox and metabolic pathways. Her research training has included four stays in the USA, in laboratories of Alabama, Yale, Pennsylvania and Harvard Universities. In 2021, she joined Dr. Kramann’s laboratory at the University Hospital RWTH Aachen, supported by a postdoctoral FEBS Long-Term fellowship, where she developed novel techniques enabling the study of metabolism in renal organoids. She now aims to decipher novel metabolism-oriented immunotherapeutic approaches based on the mitochondrial rewiring of macrophages.

This information was published in 2023, if you need updated information, please contact the award winner.

Dr. Anna Gioran carried out her graduate training at the German Center of Neurodegenerative Diseases (DZNE) in Bonn, Germany. During this time, she studied the effects of mitochondrial deficiency on the morphology of the nematode’s neurons. In her first postdoctoral fellowship she continued at the DZNE and she focused more on mitochondrial deficiencies and specifically on their metabolic implications and manners to rescue its detrimental effects at organismal level. At the moment, she is conducting postdoctoral research in the group of Dr. Niki Chondrogianni at the National Hellenic Research Foundation in Athens, Greece, focusing on the interplay between proteostatic mechanisms and mitochondrial function.

This information was published in 2023, if you need updated information, please contact the award winner.

Dr. Pedro Gonzalez Menedez fulfilled his PhD training in Dr. Rosa Sainz’s group at the University of Oviedo. His thesis, supported by the FPU program (Spanish Government), focused on GLUT transporters' role during prostate cancer progression. On the one hand, he described for the first time the expression of the insulin-dependent GLUT4 in prostate cancer cells (Endocrinology, 2014). In a second article, he found that androgen-sensitive cells are more resistant to glucose deprivation-dependent cell death by overexpressing GLUT1 and protecting oxidative stress by maintaining glutathione levels (Redox Biology, 2018). As part of his predoctoral training, he was selected for a European Association for Cancer Research short stay award in the group of Naomi Taylor in the Institut de Genétique Moléculaire de Montpellier (IGMM) at the Centre National de la Recherche Scientifique (CNRS). In 2018, he joined her group as a postdoctoral researcher under the supervision of Sandrina Kinet. First, he was supported by the Clarin-COFUND EU Program ("Gobierno del Principado de Asturias", Marie Curie Action), and then through an NIH PO1 grant. He studied the impact of mitochondrial oxidative stress during late terminal erythropoiesis (Cell Reports, 2021), and the role of the hypusinated-eIF5A in mitochondrial activity during erythropoiesis (Blood, 2023). In 2022, he rejoined the University of Oviedo with a “María Zambrano” grant into the “Redox biology and metabolism in cancer” team. Since 2023, he is a researcher funded by the “Ramón y Cajal” program (Spanish Government).

This information was published in 2023, if you need updated information, please contact the award winner.