Key result
Gpr37l1 knockout alters blood pressure versus transgenic but not standard mice or human heart failure.
Why the study?
The role of GPR37L1 in blood pressure regulation and its involvement in human cardiac disease pathophysiology remain unclear.
GPR37L1 knockout does not appear to significantly alter systolic blood pressure compared to wild-type C57BL/6J mice, and its mRNA expression is unchanged in human heart failure.
GPR37L1 unlikely to regulate BP in mice; leaves open any role in human heart failure.
This study characterizes systolic blood pressure (SBP) in a Gpr37l1 knockout mouse line, which was previously reported to have ∼60 mmHg higher SBP compared with a transgenic line. We observed only a ∼27 mmHg SBP difference between the lines. However, when compared with C57BL/6J mice, knockout mice showed no difference in SBP. We also investigated GPR37L1 mRNA abundance in human hearts and observed no difference between healthy and failing heart samples.
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Mouat et al. (2021) studied Blood pressure regulation and cardiac disease. Gpr37l1 knockout vs. Transgenic line and C57BL/6J mice was evaluated on Systolic blood pressure (SBP). Gpr37l1 knockout mice showed a ~27 mmHg systolic blood pressure difference versus a transgenic line but no difference versus C57BL/6J mice, with no mRNA differences in failing human hearts.
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