Clinical and physiological strategies aimed at maintaining the integrity and function of the proteostasis network, the cellular system responsible for regulating the synthesis, folding, trafficking, and degradation of all proteins within a cell. This network includes chaperones, proteasomes, and the ubiquitin-proteasome system. Effective support is critical for cellular resilience, as disruptions in proteostasis lead to the accumulation of misfolded or aggregated proteins, a hallmark of cellular aging and neurodegenerative diseases. Supporting this network is a fundamental strategy for longevity.
Origin
The term originates from molecular biology and cell biology, with “proteostasis” being a portmanteau of protein and homeostasis. The concept gained prominence in the early 21st century as researchers realized the interconnectedness of protein quality control mechanisms. Clinical “support” reflects the therapeutic application of this knowledge, utilizing compounds and interventions that enhance the capacity of the cell’s natural protein maintenance machinery.
Mechanism
Support mechanisms function by enhancing the expression and activity of key components within the network. This includes upregulating heat shock proteins (chaperones) that assist in proper protein folding and preventing aggregation. It also involves optimizing the autophagic and lysosomal pathways responsible for clearing damaged or misfolded proteins and organelles. By reducing proteotoxic stress, the cell can maintain functional protein pools, ensuring optimal enzyme activity and signal transduction necessary for all physiological processes.
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