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It was shown that aged or/and damaged RBCs are sequestrated in the hepatic sinusoid in a PS-dependent way, and the human sinonasal epithelial cells (HSECs) mediate the recognition and the binding of damaged RBCs in a PS-dependent manner via stabilin-1 and stabilin-2 (pro-phagocytic signals and ligandligand interactions) [275,276,277]
This dual-mechanism approach is investigated for its ability to preserve natural HPA-axis feedback while achieving greater GH/IGF-1 output than either peptide alone
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