Home Chairs: Daria Ilatovskaya, PhD - Medical College of Georgia at Augusta University, USA & Oleg Palygin, PhD - Medical University of South Carolina, USA
Kidney disease is a global health crisis, affecting millions and leading to severe cardiovascular complications. Understanding its molecular mechanisms is essential for developing targeted therapies and improving early disease detection. The kidney is a highly metabolically active organ with significant energy demands due to its role in filtration, reabsorption, and secretion. Thus, renal function is critically dependent on redox homeostasis, mitochondrial integrity, and reactive oxygen species regulation. Despite this, renal redox mechanisms remained underrepresented in mainstream SFRBM conference discussions in recent years. This symposium seeks to bridge this gap by bringing together leading experts in oxidative stress, mitochondrial dysfunction, and redox signaling in kidney disease. These talks will emphasize how disrupted redox balance contributes to kidney dysfunction by integrating emerging data on genetic susceptibilities and novel biomarkers. We expect that the symposium will foster new research directions and potential therapeutic strategies.
Invited Speakers:
Emerging Roles of Xanthine Oxidoreductase in Chronic Kidney Disease
Ilse Daehn, PhD - Icahn School of Medicine at Mount Sinai, USA
Nicotinamide Adenine Dinucleotide (NAD+) Biosynthetic Impairment in Acute Kidney Injury
Samir Parikh, PhD - UT Southwestern Medical Center, USA
Chairs: Svetlana Lutsenko, PhD - Johns Hopkins, USA & Masuko Ushio-Fukai, PhD - Medical College of Georgia at Augusta University, USA
Copper (Cu) is an essential trace element that plays a pivotal role in redox signaling and metabolic regulation. It serves as a cofactor for key enzymes involved in mitochondrial respiration, antioxidant defense, and extracellular matrix remodeling. Dysregulation of Cu homeostasis contributes to oxidative stress, inflammation, and metabolic dysfunction, which are critical drivers of cancer and cardiovascular disease. Cu transport proteins, including CTR1, ATP7A, ATP7B, and Cu chaperone Atox1, tightly regulate intracellular Cu levels to maintain cellular function. Misregulation of Cu transport can lead to increased oxidative stress and inflammatory responses. Recent discoveries in Cu biology have revealed direct Cu binding at non-catalytic sites within signaling molecules that modulate cell proliferation via the protein kinases MEK1/2, lipid metabolism via the phosphodiesterase PDE3B, and nutrient/metabolic signaling via the autophagic kinases ULK1/2. These findings established that Cu is a critical mediator of intracellular signaling. In cancer, elevated Cu levels promote angiogenesis, tumor growth, and metastasis. Similarly, in cardiovascular disease, Cu transport proteins modulate vascular function, redox balance, angiogenesis and atherosclerosis, implicating Cu as a critical regulator of vascular disease. Recent findings highlight Cu’s role in “cuproptosis”, a novel form of excess mitochondrial Cu-dependent cell death. By integrating insights from basic and translational research, this session will highlight Cu’s role as a key redox and metabolic signaling mediator and potential therapeutic target in cancer and cardiovascular disease.
Invited Speakers:
Novel Approaches for Mapping Copper Signaling in vitro and in vivo Systems
Christopher Chang, PhD - Princeton University, USA
Copper Transport Proteins as Mediators of Redox/Metabolic Signaling and Cuproptosis in Vascular Disease
Tohru Fukai, PhD - Medical College of Georgia at Augusta University, USA
Chairs: Alexsandro Figueiredo - Federal University of Rio de Janeiro, Brazil & Clint Upchurch - University of Virginia, USA
Redox biology plays a fundamental role in health and disease, with oxidative stress being a key driver in conditions such as neurodegenerative disorders, cancer, and inflammatory diseases. While traditional antioxidant therapies have shown limited clinical success, recent advances in medicinal chemistry and drug discovery are opening new avenues for modulating redox pathways beyond direct free radical scavenging. This symposium will highlight cutting-edge strategies in medicinal chemistry and drug development aimed at targeting key redox regulators such as the Keap1-Nrf2 system, thioredoxin, peroxiredoxins, and other oxidative stress-related pathways. This program will bring together experts in drug design, fragment-based discovery, structure-based drug development, and high-throughput screening to discuss innovative approaches for identifying small molecules that selectively modulate redox signaling. A major focus will be on the challenges and opportunities in developing noncovalent and covalent inhibitors of redox-related protein-protein interactions, optimizing pharmacokinetic properties of redox-modulating compounds, and leveraging computational and biophysical tools to accelerate drug discovery. Case studies will illustrate how medicinal chemistry principles have been applied to refine antioxidant therapeutics, moving beyond generic radical scavengers toward precise, pathway-specific interventions. By bridging fundamental redox biology with modern drug development strategies, this symposium aims to redefine how we approach oxidative stress-related diseases, ultimately paving the way for more effective and targeted antioxidant-based therapeutics.
Invited Speakers:
Targeting KEAP1 by Fragment-based Drug Discovery to Reduce Oxidative Stress and Inflammation
Anders Bach, PhD - University of Copenhagen, Denmark
KEAP1 Mutation Fuels Oncolytic Virotherapy in Lung Cancer by Altering Antiviral Innate Immunity and Glutamine Metabolism
David Olagnier, PhD - Aarhus University, Denmark
Chairs: Markus Waldeck-Weiermair - Brigham and Women's Hospital, USA & Paraskevi Kritsiligkou, PhD - University of Liverpool, UK
The balance of the principal cellular oxidant hydrogen peroxide (H2O2) is precisely regulated by a network of pro- and anti-oxidant oxidoreductases across different cell organelles. NADPH oxidase (NOX) isoforms are a class of enzymes with the unique function of generating either H2O2 directly or via superoxide (O2-) conversion. Dysregulated NOX activity has been strongly associated with the pathogenesis of various diseases, including cardiovascular disorders, diabetes, inflammation, cancer, and aging. However, recent research underscores the physiological significance of intracellular oxidants in orchestrating key signaling pathways that govern angiogenesis, vascular permeability, cell proliferation, differentiation, and gene regulation. NOX isoforms are differentially expressed among cell types and differentially distributed within distinct subcellular membranes. Likewise, H2O2 concentration levels greatly vary among cell compartments. Little is known of how and in which subcellular locales H2O2 gets generated by distinct NADPH oxidases in response to environmental stressors as well as to receptor-dependent modulations. Moreover, recent research suggests that NOX isoforms are interconnected, thus controlling compartmentalized H2O2 levels for modulating diverse cell organelle functions such as mitochondrial metabolism, ER protein folding, or gene expression. Understanding the intricate mechanisms by which NOX isoforms mediate intra- and intercellular redox signaling is essential for elucidating ROS-mediated cellular communication. This session will examine the most recent discoveries on the generation of localized H2O2 by NADPH oxidases with a specific focus on the roles of NOX4 in vivo and in primary endothelial cells.
Invited Speakers:
Roles of Localized ROS Generation from Stress Adaptation to Sexual Dimorphism
Siobhan Craige, PhD - Virginia Tech, USA
Dynamic Regulation of Receptor-modulated Endothelial NADPH Oxidases
Markus Waldeck-Weiermair, PhD - Brigham and Women's Hospital, USA
Chairs: Bradford Hill, PhD - University of Louisville, USA & Victor Darley-Usmar, PhD - University of Alabama at Birmingham, USA
Over the past 3.8 billion years, evolution has driven life forward through metabolism—one of its engines of biological adaptation. Once considered a mere permissive requirement for life, emerging evidence now reveals metabolism as a powerful force shaping physiology and phenotypic change. Dietary and physical activity-driven metabolic shifts can enhance tissue adaptation and promote health, while metabolic dysfunction can trigger pathological remodeling, fueling disease. Understanding how metabolism senses and integrates environmental cues is therefore critical for developing targeted therapies to improve human health. At its core, metabolism operates through redox reactions, making redox biochemistry fundamental to health and disease. Yet, key challenges remain in deciphering how genetic and environmental factors intersect to shape metabolic health, how exercise-induced metabolic shifts enhance well-being, how metabolism influences immune responses, and how aging impacts metabolic and redox processes. Recent advances in metabolomics, redox indicators, and bioinformatics offer unprecedented opportunities to tackle these questions, deepening our understanding of fundamental mechanisms while accelerating translational breakthroughs. Accordingly, this session brings together researchers on the cutting edge of metabolic research, with the speakers organized to crystallize current knowledge and yield emerging questions.
Invited Speakers:
Metabolic Regulation of Redox State and Vascular Physiology
Matthew Nystoriak, PhD - Masonic Medical Research Institute, USA
Differential Bioenergetic Metabolite Interactomes Associated with Clinical Profiles in Asthma Patients
Serpil Erzurum, PhD - Cleveland Clinic, USA
Chairs: Kimberly Dunham-Snary, PhD - Queen's University, Canada & Mia Wilkinson - Queen's University, Canada
Extracellular vesicles (EVs) are emerging as critical mediators of intercellular communication, with significant implications for redox biology, disease pathology, and therapeutic intervention. These membrane-bound vesicles carry bioactive molecules—including proteins, lipids, and nucleic acids—that influence oxidative stress responses and metabolic programming in recipient cells. Recent advances in EV research have highlighted their dual role as both biomarkers and modulators of redox signaling pathways in cardiovascular disease, ischemia-reperfusion injury, and inflammatory disorders. This symposium will explore cutting-edge findings on EV-mediated redox regulation, focusing on their potential as therapeutic agents. Dr. Ruhul Abid will present his work on hypoxia-conditioned EVs and their role in modulating oxidative stress and promoting angiogenesis in ischemic myocardium. Dr. Éric Boilard will explore the role of platelet-derived EVs in inflammatory responses and vascular health. Additionally, an alternate presentation from Dr. Yajing Wang will discuss how EVs contribute to cardiovascular disease progression, particularly through their interactions with mitochondria and oxidative stress pathways. By integrating perspectives from cardiovascular biology, immunology, and redox research, this session will provide a comprehensive overview of EVs as both regulators and potential therapeutic tools in oxidative stress-related diseases. The insights gained from this session will contribute to the broader understanding of redox mechanisms and interdisciplinary approaches to targeting EV pathways for disease treatment.
Invited Speakers:
Platelet EVs in Lymphatic Redox Homeostasis
Catherine Martel, PhD - Université Laval/CHU de Québec, Canada
Cardiosphere-Derived EVs Activate Nrf2-Mediated Antioxidant Defenses
Eduardo Marbán, PhD - Cedars Sinai Medical Center, USA
Chairs: Rebecca Oberley-Deegan, PhD - University of Nebraska Medical Center, USA & Phyllis Dennery, MD - Brown University, USA
Senescence is increasingly recognized as a significant contributor to the development and progression of various diseases. As cells enter senescence, they undergo profound changes in gene expression, secreting a complex mixture of bioactive molecules known as the senescence-associated secretory phenotype (SASP), which can create a pro-inflammatory microenvironment, promoting chronic inflammation, tissue dysfunction, and ultimately contributing to the pathogenesis of several diseases. Senescence has been implicated in the development of conditions such as cancer, neurodegenerative disorders, cardiovascular diseases, and metabolic disorders. Elevated levels of ROS, including superoxide and hydrogen peroxide, induce DNA damage, trigger cellular stress responses, epigenetic changes and activate signaling pathways leading to senescence. The intricate interplay between ROS and senescence highlights the complex relationship between cellular redox status and the regulation of many diseases, making these processes subjects of intense research in understanding potential therapeutic interventions.
Invited Speakers:
Selenium, Senescence and Cancer Inhibition
Andrés Melendez, PhD - University of Albany, USA
Senescence as a Driver of Aging and Acute Injury
Raghavan Raju, PhD - Augusta University, USA
Chairs: Francisco Laurindo, MD, PhD - Universidade de São Paulo, Brazil & Andrea Mattevi, PhD - University of Pavia, Italy
Recent developments in redox biology reinforced their crucial involvement in cellular processes and their implications for health and disease. Technical advances and novel conceptual insights have indeed provided a deeper understanding of how redox regulation affects cellular behavior, with most such studies focusing mainly on biochemical aspects of protein modifications. However, the precise molecular mechanisms whereby redox processes affect overall protein function and associated cellular processes are not well understood. It is now becoming apparent that physical or physicochemical processes interact with cell signaling and, in particular with redox-dependent molecular modifications, both at molecular and systems levels. Our proposal intends to specifically address the mechanisms underlying the interplay between redox processes and their associated chemistry with the physical biology of redox-modified proteins, focusing on processes such as molecular mechanisms of oxygen sensing and liquid phase separation, among others. We propose that an integrated discussion on how redox protein modifications affect not only protein structure and stability but also their physical behavior will be very stimulating and forward-thinking, bringing state-of-the-art emerging knowledge to enrich the understanding of redox science.
Invited Speakers:
N-terminal Cysteine Acetylation and Oxidation as a Universal Mechanism of Oxygen Sensing
Emily Flashman, PhD - Oxford University, UK
Protein Thiol Alterations Drive Aberrant Phase Separation in Aging
Milos Filipovic, PhD - Leibniz Institute for Analytical Sciences, Germany
Chairs: Priyamvada Rai, PhD - University of Miami, USA & Brian Cunniff, PhD - University of Vermont, USA
Redox biology and metabolism are crucial for understanding cancer development and progression as cancer cells significantly alter their metabolic processes to fuel rapid proliferation. This metabolic reprogramming is tightly linked to redox balance, where the production and neutralization of reactive oxygen species (ROS) play a pivotal role in tumor initiation, growth, invasion, and resistance to therapy. Redox balance is a potent Achilles heel for tumors as maintaining a pro-proliferative redox state while suppressing oxidative damage is critical for cancer cells to survive and thrive in the evolving tumor environment. The speakers are experts in novel therapeutically relevant targets in cancer, understanding the role of oxidative stress in metastatic phenomenon, and in vivo models of key redox protective pathways in cancer development and progression.
Invited Speakers:
The Role of Antioxidant Proteins in Cancer Onset and Progression
Isaac Harris, PhD - University of Rochester, USA
Reversible Redox Switches in Cancer Progression
Christine Chio, PhD - Columbia University, USA
Chairs: Maria Carmen Gomez-Cabrera, PhD - University of Valencia, Spain & Giovanni Mann, PhD - Kings College London, UK
Research in redox biology of exercise has made considerable advances in the last 70 years. Since the seminal study of George Pake's group calculating the content of free radicals in skeletal muscle in resting conditions in 1954 (Commoner et al., 1954), many discoveries have been made in the field. Physical exercise increases the cellular production of reactive oxygen species (ROS). Initially, ROS were considered detrimental and thus a likely cause of exhaustion-related cell damage. In the last decade, however, evidence has shown that ROS acts as signals mediating different muscle adaptations in exercise. Thus, the idea that antioxidant supplementation in exercise is always recommendable has proved incorrect (Gomez-Cabrera et al., 2008; Gomez-Cabrera et al., 2020). During this symposium, we will discuss state-of-the-art contributions in redox biology, sources of ROS in skeletal muscle, the importance of oxidants and antioxidants, and the balance between them in exercise-induced adaptations in young and old populations. Dra. Gomez-Cabrera will discuss the role of ROS in exercise-induced muscle damage and its effects on muscle adaptations to exercise. She will also show data on muscle repair mechanisms in exercised young and old mice and humans with translational impact in age-associated diseases (Roman et al., 2021; Lai et al., 2024). Based on results from human and rodent studies, Dr. Lanner will give molecular insight into how increased ROS production can exert beneficial and detrimental effects on skeletal muscle function. The outcome depends on a combination of factors, including the type of ROS, the magnitude, duration, and location (mitochondria, cytosolic) of ROS production, and the defense systems, including both endogenous and exogenous antioxidants (Liu et al., 2021; Steinz et al., 2024).
Invited Speakers:
Role of Redox Signaling in Skeletal Muscle Damage An Adaptation to Training in Young and Old Populations
Maria Carmen Gomez-Cabrera, PhD - University of Valencia, Spain
Elucidating Inflammation-induced Mitochondrial Deficiency in Skeletal Muscle
Johanna Lanner, PhD - Karolinska Institutet, Sweden
Chairs: Jason Hansen, PhD - Brigham Young University, USA & Craig Harris, PhD - University of Michigan, USA
Redox systems exist to maintain a level of control that permeates through several processes that support various aspects of life. Not surprisingly, the role of redox signaling and control is also evident in a fundamental, basic tenet of life, reproduction and development. Development is characterized by a strict coordination of specific cellular events, such as proliferation, differentiation and apoptosis, within a specific timeframe. Timely redox control of sensitive elements is critical as disruption can lead to poor developmental outcomes, such as functional deficits, dysmorphogenesis or spontaneous embryonic death. Newer evidence supports specific redox-sensitive elements that point to control within nearly every stage of development, from the determination of early cell fate to the post-implantation supervision of organogenesis. Speakers assembled in this session will address basic and advanced concepts within the fields of developmental biology and toxicology that are specifically related to redox biology.
Invited Speakers:
The Redox Theory of Development
Craig Harris, PhD - University of Michigan, USA
Redox Regulation of Stem Cell Fate During Development
Agnes Ulfig, PhD - University of Iceland, Iceland
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