Society for Free Radical Research - Europe

More info about the "SFRR-E ECR Subcommittee"

We are pleased to announce the recipients of the 2023 round of SFRR-E / Oxygen Club of California (OCC) Early Career Researcher (ECR) Fellowships.

The ECR Fellowships are specifically for researchers under 40 years of age, who are working in different areas of biological sciences and medicine working in the redox biology field. They are intended to provide ECRs support of up to €10,000 for research or seed-funding for a new project, which should be relevant to the field of redox research and completed within a 12-month period. 

Sophie Hendrix. Hasselt University (Belgium)

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.

Project title: SUPPRESSOR OF GAMMA RESPONSE 1 – A novel mediator of oxidative signalling in plants?

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

VERÓNICA MIGUEL. Spanish National Centre for Cardiovascular Research

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.

Project title: Boosting fatty acid oxidation to target macrophage function: role of mitochondrial reactive oxygen species.

Project title: Boosting fatty acid oxidation to target macrophage function: role of mitochondrial reactive oxygen species. Macrophages are essential cells of the innate immune system that respond to an infection or accumulation of damaged and dead cells to maintain tissue homeostasis. Reactive oxygen species (ROS) play critical roles in macrophage activation and functions by regulating signal transduction and gene expression pathways. In turn, mitochondrial metabolic adaptations have emerged as effectors of macrophage responses. While fatty acids constitute one of the main substrates of mitochondria and the electron leakage of the respiratory chain is a key source of ROS, the role of fatty acid oxidation (FAO) and associated mitochondrial ROS on macrophage function is still poorly understood. To address this, we will generate a new mouse model with enhanced FAO in macrophages and will analyze the impact of this reprogramming on its biology. This knowledge will provide a firm basis for novel metabolism-oriented immunotherapeutic approaches.

Anna Gioran. National Hellenic Research Foundation in Athens, Greece

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.

Project title: The role of UPRER and mitochondria in proteasome activation-induced longevity in C. elegans

Project title: The role of UPRER and mitochondria in proteasome activation-induced longevity in C. elegans Proteins are the main executors of cellular functions. Proteins also become damaged with ageing or toxic exposure and eventually, dysfunctional. The cell has protective mechanisms against dysfunctional proteins, often resorting to protein destruction. One of these mechanisms is the proteasome, a large and complex molecule, its function resembling that of a document shredder. The proteasome’s capacity to destroy damaged proteins wears off with ageing. Work from our group shows that if the proteasome remains active with age or gets activated, then cells or even entire organisms remain young and healthy and live longer. Currently, we do not know the reasons behind this phenomenon but understanding them more deeply will help researchers plan effective anti-ageing approaches. This work has so far shown that proteasome activation engages other protective mechanisms of the cell that are normally activated when a cell or an organism faces dangerous or stressful stimuli. These mechanisms seem to be crucial in extending the lifespan of organisms with an activated proteasome. These findings are vital if we want to apply the knowledge of how the manipulation of the proteasome extends organismal lifespan in the design of anti-ageing strategies.

Pedro Gonzalez Menedez. University of Oviedo (Spain)

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).

Project title: Crosstalk between the redox regulation of erythropoiesis and diabetes

 Anemia –defined as a low number of healthy erythrocytes– is one of the most common blood-related disorders in patients with diabetes. The bridge between erythroid development and diabetes is not understood in patients who present with a physiological production of erythropoietin. Mitochondrial ROS signal is required for erythropoiesis. Moreover, the loss of this critical mitochondrial ROS signal inhibits the EPO signalling that is required for RBC production. Thioredoxin-interacting protein (TXNIP), in addition to a critical role in cellular redox control by thioredoxin, act as main regulator of metabolism through pleiotropic actions. TXNIP depletion protects from diabetes, and it is a target of erythropoietin. The aims of this project are: 1) Evaluate the role of mitochondrial stress, caused by a high glucose and low insulin on diabetes-induced anemia and 2) Investigate the impact of a new anti-diabetic compound (SRI-37330) that targeted TXNIP on erythroid differentiation. The results obtained will allow us to determine whether impacting the redox signaling modulates erythroid differentiation during diabetes. In conclusion, deciphering the redox dialogue between diabetes and anemia will open new avenues for the development of novel therapeutic strategies.


The Society for Free Radical Research - Europe (SFRR-E) is dedicated to promoting interest in all aspects of research related to Free Radicals in any scientific field.


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