Proteostasis collapse across the lifespan

Protein homeostasis, or proteostasis, is essential for maintaining the synthesis, folding, trafficking, and degradation of proteins throughout the lifespan. Aging is associated with a progressive decline in proteostasis capacity, resulting in the accumulation of misfolded and aggregated proteins, impaired cellular adaptation to stress, and reduced tissue function. This decline is implicated in age-related disorders, including neurodegenerative disease, sarcopenia, metabolic dysfunction, and cardiovascular disease. Although substantial progress has been made in understanding molecular chaperones, autophagy, the ubiquitin-proteasome system, and stress-response pathways, important questions remain about how proteostasis networks deteriorate across tissues and life stages, how these pathways interact, and why some cells and organisms maintain proteome stability more effectively than others. A better understanding of these processes may reveal mechanisms that link proteostasis failure to aging and identify opportunities for therapeutic intervention.This Research Topic aims to advance mechanistic understanding of proteostasis decline across the lifespan. It will bring together studies examining how protein synthesis, folding, quality control, trafficking, and degradation are coordinated during aging, as well as how their disruption contributes to cellular dysfunction and age-related disease. We particularly welcome research addressing interactions between intracellular and inter-tissue proteostasis networks, differences in proteostasis resilience between cell types and organisms, and strategies for preserving or restoring proteome integrity. Studies may also explore whether interventions that target proteostasis can extend healthspan, delay disease progression, or improve tissue repair and function in later life.To gather further insights into the molecular and cellular mechanisms of proteostasis collapse during aging, this Research Topic welcomes articles addressing, but not limited to, the following themes:- Molecular chaperone networks and the heat-shock response in aging- Autophagy, lysosomal function, and the ubiquitin-proteasome system- Regulation of protein synthesis, folding, trafficking, and degradation across the lifespan- Cell-autonomous, non-cell-autonomous, and inter-tissue proteostasis signalling- Proteostasis decline in neurodegeneration, sarcopenia, metabolic disease, and other age-related conditions- Protein aggregation, proteotoxic stress, and cellular stress responses- Multi-omics, imaging, and systems-level approaches to proteostasis research- Single-cell, spatial, and computational approaches to dissecting cell-type-specific proteostasis dynamics and cellular heterogeneity in aging- Genetic, pharmacological, dietary, and lifestyle interventions that preserve proteostasis- Biomarkers of proteostasis capacity, dysfunction, and biological aging- Comparative and evolutionary perspectives on proteostasis resilienceWe welcome original research, reviews, and perspectives that advance mechanistic understanding of proteostasis in aging and its translational potential. Topic editors: Saisai Wei, Xiangwei Gao, Xinhui Wang Source: https://www.frontiersin.org/research-topics/86070/proteostasis-collapse-across-the-lifespan