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Malignant tumors are characterized by diverse metabolic stresses, including nutrient shortages, hypoxia, and buildup of metabolic by-products. To understand how cancer cells adapt to such challenges, ...

Martinez-Martinez et al. combine a host-microbe-drug-nutrient screen with multi-omics to reveal how the cancer-associated microbiota modulates chemotherapy. They identify 2-methylisocitrate, a microbi...

CroAge Project, Founded by the Europe Union

It is widely accepted that susceptibility to infection increases with age. The reason often invoked is the dysregulation of the immune system, which is both cause and consequence of ageing. However, w...

Redox signalling is emerging as an important regulator of metabolism and physiology, which is dysregulated in ageing and disease. Here, the authors show that redox regulation of a key redox sensitive ...

Research Associate (Fixed Term) in the Department of Genetics at the University of Cambridge.

Peroxiredoxins are highly conserved thiol peroxidases essential for peroxide detoxification, redox signaling, and chaperone activity. Prx1/AhpC-type peroxiredoxins are found throughout the eukaryotic ...

Skeletal muscle fatigue occurs, in part, from accumulation of hydrogen (H+) and phosphate (Pi); however, the molecular basis through which these ions inhibit function is not fully understood. Therefore, we examined the effects of these metabolites on myosin-actin cross-bridge kinetics and mechanical properties in skeletal muscle fibers from older (65-75 years) adults. Slow-contracting myosin heavy chain (MHC) I and fast-contracting MHC IIA fibers were examined under control (5 mM Pi, pH 7.0) and fatigue (30 mM Pi, pH 6.2) conditions at maximal calcium-activation (5 mM ATP) and rigor (0 mM ATP). In MHC I and IIA fibers, fatigue decreased force per fiber size (23-37%), which was accompanied by reduced strongly bound myosin head characteristics (number and/or stiffness; 21-47%) and slower cross-bridge kinetics (longer myosin attachment times (22-46%) and reduced rates of force production (20-33%)) compared with control. MHC I myofilaments became stiffer with fatigue, a potential mechanism to increase force production. In rigor, which causes the myosin that can bind actin to be strongly bound, fatigue decreased force per fiber size (32-33%) in MHC I and IIA fibers, indicating less force was generated per cross-bridge. By replacing ATP with 2-deoxy-ATP (dATP), the fatigue-induced slowing of cross-bridge kinetics in MHC I and IIA fibers was reversed and reduced force production in MHC I fibers was partially improved, revealing potential mechanisms to help mitigate fatigue in older adults. Overall, our results identify novel fiber type-specific changes in cross-bridge kinetics, force per cross-bridge, and myofilament stiffness that help explain fatigue in older adults.

Nature Metabolism, Published online: 03 March 2025; doi:10.1038/s42255-025-01225-wZuhra and Petrosino et al. report evidence that cyanide acts as a regulatory gasotransmitter in mammalian cells, where it is shown to affect cellular bioenergetics, most…

Advanced proteomic organ ageing is associated with the long-term risk of age-related diseases. In most cases, faster ageing of a specific organ increases susceptibility to morbidity affecting multiple...

Tang, Yue, Xu and colleagues map the proteome of several thousand individuals over a 9-year period to identify potential biomarkers of ageing and of age-associated diseases.

This Consensus Statement provides a nomenclature framework and experimental recommendations for studying mitochondrial transfer and transplantation.

Blocking the activity of a protein called p21 stops lung cancer cells entering a ‘sleep-like’ state that allows them to survive chemotherapy. Blocking p21 causes more cancer cells to die and reduces t...