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These categories included genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication [2]
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References appear solely for educational comparison regarding GLP-1 and GIP mechanisms
and (4) growth hormone receptor upregulation at injury sites, restoring local GHR density without elevating systemic GH levels
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