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In fact, unlike the α 2A - and α 2B - subtypes, α 2C -ARs do not exhibit decreases in agonist binding affinity (Eason and Liggett, 1992) or β AR kinase 1 (GRK2) mediated phosphorylation (Kurose and Lefkowitz, 1994)
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The block in bench-to-bedside translation may in part be due to a lack of pre-clinical HFpEF models that adequately recapitulate heterogeneity of the human condition
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