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Although inflammation is usually considered primarily associated to atherosclerotic CVD, it is also strongly bound to heart failure with preserved ejection fraction (HFpEF)

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This increase in DAT function stems at least in part from augmented DAT surface expression, pointing to DAT trafficking as the underlying mechanism by which GLP-1R signaling and AA levels controls DA homeostasis in the LS, as depicted by our schematic model (Supplementary Figure 5)

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The GLP-1R has been previously reported to follow a dynamin-dependent, but either clathrin-mediated (CME) or clathrin-independent (CIE) endocytosis pathway (7173), which represent the two main mechanisms underlying receptor endocytosis