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& Gallwitz, B

This is further supported by the near-complete absence of cardiac Glp1r mRNA in Glp1r Tie2/ mice (57), suggesting that mouse cardiac Glp1r expression is primarily contributed by endothelial cells and/or immune cells

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Lastly, we discuss the evidence in support of the hypothesis that the neuroprotective effects of long-term GLP-1RAs may partly be mediated by improved neurovascular coupling, and conclude with outlining some aspects as the outstanding questions

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