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Most evidence to date reflects changes in downstream or adaptive pathways, such as inflammation, mitochondrial function, and metabolic regulation, rather than direct modification of the primary sources of molecular damage

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Its substrates also include pituitary adenylate cyclaseactivating polypeptides, insulinlike growth factor1, peptide YY, substance P, neuropeptide Y, gastrinreleasing polypeptides, and several chemokines, indicating its role in additional homeostatic functions, such as neurogenic inflammation, blood pressure control, and immune regulation [41]