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As representative molecular chaperones, HSPs can regulate conformational changes by promoting correct protein folding and refolding, repair denatured proteins, prevent misfolding, and maintain cellular homeostasis, thus protecting the host [14]

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However, in PEM patients, due to a lack of effective negative feedback regulation (e.g., compromised antioxidant capacity and impaired mitochondrial autophagy), these responses fail to resolve post-exercise, thereby potentially progressing into a chronic pathological state (105) ( Figure 2 )

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