Dr. Afshin Beheshti 
 

Bio:
Afshin Beheshti, PhD is a Professor of Surgery and of Computational & Systems Biology at the University of Pittsburgh School. He serves as Director of the newly launched Space Center for Space Biomedicine and as Associate Director of the McGowan Institute for Regenerative Medicine at Pitt​. In addition, Dr. Beheshti holds a visiting scientist appointment at the Broad Institute of MIT and Harvard​.

Abstract:
Human spaceflight presents significant health challenges driven by microgravity, space radiation, isolation, and other environmental stressors. Recent multi-omics research has revealed that mitochondrial dysfunction is a central biological consequence of space travel, contributing to systemic impacts such as accelerated aging, cardiovascular disease, and impaired metabolic function. Data from astronaut missions and ground-based space analogs demonstrate persistent mitochondrial suppression even after returning to Earth. This talk highlights how space serves as a unique accelerated model for studying human diseases and aging, offering insights applicable both to space exploration and terrestrial medicine. Using advanced 3D organoid models and multi-omics analysis, we have identified promising countermeasures, including the natural flavonoid Kaempferol, which restores mitochondrial bioenergetics and reverses radiation-induced gene expression changes in multiple tissues. These findings underscore the critical role of mitochondria as both biomarkers and therapeutic targets for sustaining human health in deep space missions, while also advancing precision medicine strategies on Earth.

Dr. Afshin Beheshti 
 

Bio:
Afshin Beheshti, PhD is a Professor of Surgery and of Computational & Systems Biology at the University of Pittsburgh School. He serves as Director of the newly launched Space Center for Space Biomedicine and as Associate Director of the McGowan Institute for Regenerative Medicine at Pitt​. In addition, Dr. Beheshti holds a visiting scientist appointment at the Broad Institute of MIT and Harvard​.

Abstract:
Human spaceflight presents significant health challenges driven by microgravity, space radiation, isolation, and other environmental stressors. Recent multi-omics research has revealed that mitochondrial dysfunction is a central biological consequence of space travel, contributing to systemic impacts such as accelerated aging, cardiovascular disease, and impaired metabolic function. Data from astronaut missions and ground-based space analogs demonstrate persistent mitochondrial suppression even after returning to Earth. This talk highlights how space serves as a unique accelerated model for studying human diseases and aging, offering insights applicable both to space exploration and terrestrial medicine. Using advanced 3D organoid models and multi-omics analysis, we have identified promising countermeasures, including the natural flavonoid Kaempferol, which restores mitochondrial bioenergetics and reverses radiation-induced gene expression changes in multiple tissues. These findings underscore the critical role of mitochondria as both biomarkers and therapeutic targets for sustaining human health in deep space missions, while also advancing precision medicine strategies on Earth.

Dr. Afshin Beheshti 
 

Bio:
Afshin Beheshti, PhD is a Professor of Surgery and of Computational & Systems Biology at the University of Pittsburgh School. He serves as Director of the newly launched Space Center for Space Biomedicine and as Associate Director of the McGowan Institute for Regenerative Medicine at Pitt​. In addition, Dr. Beheshti holds a visiting scientist appointment at the Broad Institute of MIT and Harvard​.

Abstract:
Human spaceflight presents significant health challenges driven by microgravity, space radiation, isolation, and other environmental stressors. Recent multi-omics research has revealed that mitochondrial dysfunction is a central biological consequence of space travel, contributing to systemic impacts such as accelerated aging, cardiovascular disease, and impaired metabolic function. Data from astronaut missions and ground-based space analogs demonstrate persistent mitochondrial suppression even after returning to Earth. This talk highlights how space serves as a unique accelerated model for studying human diseases and aging, offering insights applicable both to space exploration and terrestrial medicine. Using advanced 3D organoid models and multi-omics analysis, we have identified promising countermeasures, including the natural flavonoid Kaempferol, which restores mitochondrial bioenergetics and reverses radiation-induced gene expression changes in multiple tissues. These findings underscore the critical role of mitochondria as both biomarkers and therapeutic targets for sustaining human health in deep space missions, while also advancing precision medicine strategies on Earth.

Dr. Afshin Beheshti 
 

Bio:
Afshin Beheshti, PhD is a Professor of Surgery and of Computational & Systems Biology at the University of Pittsburgh School. He serves as Director of the newly launched Space Center for Space Biomedicine and as Associate Director of the McGowan Institute for Regenerative Medicine at Pitt​. In addition, Dr. Beheshti holds a visiting scientist appointment at the Broad Institute of MIT and Harvard​.

Abstract:
Human spaceflight presents significant health challenges driven by microgravity, space radiation, isolation, and other environmental stressors. Recent multi-omics research has revealed that mitochondrial dysfunction is a central biological consequence of space travel, contributing to systemic impacts such as accelerated aging, cardiovascular disease, and impaired metabolic function. Data from astronaut missions and ground-based space analogs demonstrate persistent mitochondrial suppression even after returning to Earth. This talk highlights how space serves as a unique accelerated model for studying human diseases and aging, offering insights applicable both to space exploration and terrestrial medicine. Using advanced 3D organoid models and multi-omics analysis, we have identified promising countermeasures, including the natural flavonoid Kaempferol, which restores mitochondrial bioenergetics and reverses radiation-induced gene expression changes in multiple tissues. These findings underscore the critical role of mitochondria as both biomarkers and therapeutic targets for sustaining human health in deep space missions, while also advancing precision medicine strategies on Earth.

Dr. Afshin Beheshti 
 

Bio:
Afshin Beheshti, PhD is a Professor of Surgery and of Computational & Systems Biology at the University of Pittsburgh School. He serves as Director of the newly launched Space Center for Space Biomedicine and as Associate Director of the McGowan Institute for Regenerative Medicine at Pitt​. In addition, Dr. Beheshti holds a visiting scientist appointment at the Broad Institute of MIT and Harvard​.

Abstract:
Human spaceflight presents significant health challenges driven by microgravity, space radiation, isolation, and other environmental stressors. Recent multi-omics research has revealed that mitochondrial dysfunction is a central biological consequence of space travel, contributing to systemic impacts such as accelerated aging, cardiovascular disease, and impaired metabolic function. Data from astronaut missions and ground-based space analogs demonstrate persistent mitochondrial suppression even after returning to Earth. This talk highlights how space serves as a unique accelerated model for studying human diseases and aging, offering insights applicable both to space exploration and terrestrial medicine. Using advanced 3D organoid models and multi-omics analysis, we have identified promising countermeasures, including the natural flavonoid Kaempferol, which restores mitochondrial bioenergetics and reverses radiation-induced gene expression changes in multiple tissues. These findings underscore the critical role of mitochondria as both biomarkers and therapeutic targets for sustaining human health in deep space missions, while also advancing precision medicine strategies on Earth.

Dr. Afshin Beheshti 
 

Bio:
Afshin Beheshti, PhD is a Professor of Surgery and of Computational & Systems Biology at the University of Pittsburgh School. He serves as Director of the newly launched Space Center for Space Biomedicine and as Associate Director of the McGowan Institute for Regenerative Medicine at Pitt​. In addition, Dr. Beheshti holds a visiting scientist appointment at the Broad Institute of MIT and Harvard​.

Abstract:
Human spaceflight presents significant health challenges driven by microgravity, space radiation, isolation, and other environmental stressors. Recent multi-omics research has revealed that mitochondrial dysfunction is a central biological consequence of space travel, contributing to systemic impacts such as accelerated aging, cardiovascular disease, and impaired metabolic function. Data from astronaut missions and ground-based space analogs demonstrate persistent mitochondrial suppression even after returning to Earth. This talk highlights how space serves as a unique accelerated model for studying human diseases and aging, offering insights applicable both to space exploration and terrestrial medicine. Using advanced 3D organoid models and multi-omics analysis, we have identified promising countermeasures, including the natural flavonoid Kaempferol, which restores mitochondrial bioenergetics and reverses radiation-induced gene expression changes in multiple tissues. These findings underscore the critical role of mitochondria as both biomarkers and therapeutic targets for sustaining human health in deep space missions, while also advancing precision medicine strategies on Earth.

Dr. Deb Bell-Pedersen | Pedersen Lab

Abstract:
The circadian clock is a fundamental regulator of human health and drug metabolism, coordinating daily rhythms in protein production that affect cellular function and metabolism. Many proteins that cycle robustly are produced from non-rhythmic mRNAs, pointing to translational control as a key mechanism of rhythmic protein levels. Using the model eukaryote Neurospora crassa, we discovered that the clock exerts this regulation through rhythmic control of a conserved translation initiation factor (eIF2α) and by remodeling ribosome composition. Even more unexpectedly, we discovered that the circadian system governs the fidelity of protein synthesis by modulating ribosome makeup and tRNA synthetase activity. Both translational fidelity and circadian amplitude decline with age. We identified compounds that restore clock amplitude in old N. crassa cells, leading to improved translation accuracy and extended lifespan. These findings reveal how the circadian clock programs daily changes in the proteome beyond genomic instructions and highlight a novel link between circadian regulation, proteome integrity, and aging.

Dr. Deb Bell-Pedersen | Pedersen Lab

Abstract:
The circadian clock is a fundamental regulator of human health and drug metabolism, coordinating daily rhythms in protein production that affect cellular function and metabolism. Many proteins that cycle robustly are produced from non-rhythmic mRNAs, pointing to translational control as a key mechanism of rhythmic protein levels. Using the model eukaryote Neurospora crassa, we discovered that the clock exerts this regulation through rhythmic control of a conserved translation initiation factor (eIF2α) and by remodeling ribosome composition. Even more unexpectedly, we discovered that the circadian system governs the fidelity of protein synthesis by modulating ribosome makeup and tRNA synthetase activity. Both translational fidelity and circadian amplitude decline with age. We identified compounds that restore clock amplitude in old N. crassa cells, leading to improved translation accuracy and extended lifespan. These findings reveal how the circadian clock programs daily changes in the proteome beyond genomic instructions and highlight a novel link between circadian regulation, proteome integrity, and aging.

Dr. Deb Bell-Pedersen | Pedersen Lab

Abstract:
The circadian clock is a fundamental regulator of human health and drug metabolism, coordinating daily rhythms in protein production that affect cellular function and metabolism. Many proteins that cycle robustly are produced from non-rhythmic mRNAs, pointing to translational control as a key mechanism of rhythmic protein levels. Using the model eukaryote Neurospora crassa, we discovered that the clock exerts this regulation through rhythmic control of a conserved translation initiation factor (eIF2α) and by remodeling ribosome composition. Even more unexpectedly, we discovered that the circadian system governs the fidelity of protein synthesis by modulating ribosome makeup and tRNA synthetase activity. Both translational fidelity and circadian amplitude decline with age. We identified compounds that restore clock amplitude in old N. crassa cells, leading to improved translation accuracy and extended lifespan. These findings reveal how the circadian clock programs daily changes in the proteome beyond genomic instructions and highlight a novel link between circadian regulation, proteome integrity, and aging.

Dr. Deb Bell-Pedersen | Pedersen Lab

Abstract:
The circadian clock is a fundamental regulator of human health and drug metabolism, coordinating daily rhythms in protein production that affect cellular function and metabolism. Many proteins that cycle robustly are produced from non-rhythmic mRNAs, pointing to translational control as a key mechanism of rhythmic protein levels. Using the model eukaryote Neurospora crassa, we discovered that the clock exerts this regulation through rhythmic control of a conserved translation initiation factor (eIF2α) and by remodeling ribosome composition. Even more unexpectedly, we discovered that the circadian system governs the fidelity of protein synthesis by modulating ribosome makeup and tRNA synthetase activity. Both translational fidelity and circadian amplitude decline with age. We identified compounds that restore clock amplitude in old N. crassa cells, leading to improved translation accuracy and extended lifespan. These findings reveal how the circadian clock programs daily changes in the proteome beyond genomic instructions and highlight a novel link between circadian regulation, proteome integrity, and aging.