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Cellular metabolism and stress-response pathways represent a broad and integrated network of biochemical processes and signaling cascades that maintain cellular homeostasis and enable adaptation to environmental stressors. These pathways include primary metabolic routes such as glycolysis and oxidative phosphorylation, as well as adaptive mechanisms like the Integrated Stress Response (ISR), the heat shock response, and the unfolded protein response (UPR) [1][2]. In many diseases, these pathways are hijacked or dysregulated; for instance, cancer cells often undergo metabolic reprogramming to support rapid proliferation, while neurodegenerative diseases are frequently characterized by chronic stress-response activation due to protein misfolding [3][4]. Because this term describes a collection of pathways rather than a single protein or receptor, it is not considered a specific therapeutic target in itself. However, individual components within these pathways, such as AMPK, mTOR, or PERK, are major focal points for drug development. Therapeutic agents like Metformin and Rapamycin are widely used to modulate these metabolic and stress-related nodes to treat conditions ranging from type 2 diabetes to various malignancies [5][6].
Modulation of specific enzymes and signaling nodes (e.g., AMPK activation, mTOR inhibition, or ISR modulation) to restore metabolic homeostasis or induce selective cell death in stressed environments.
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