S1PR1 and myocardial infarction: Whereas, long-term overexpression of S1PR1 as a result of gene therapy in chronic HF post-MI in Sprague Dawley rats resulted in significantly smaller LV internal diastolic diameter, lower LV end diastolic pressure, and higher systolic and diastolic function, which reduced the infiltration of immune cells and restored the total plasma membrane β-adrenergic receptor (βAR) density in comparison with the HF controls with physiologically lower myocardial expression of S1PR1.