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Alanine mutations for four of the selected residues (Ile323, Val160, Gly151, and His363) were predicted to cause changes in the GLP-1R structure in the active state by altering the cavity or causing changes in exposed residues and breakages in salt bridges between residues, while a further three alanine mutated residues (Val229, Gly151, and His363) were predicted to cause changes in the inactive GLP-1R structure (Figure 2G)

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Astrocyte deficiency significantly disrupts vascular repair and remodeling, impairing motor function recovery after stroke and underscoring their crucial reparative role [156]

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