Key result
PAGly activates ventricular adrenergic signaling less efficiently than selective agonists, potentially blunting sympathetic stimulation.
Why the study?
Does phenylacetylglycine (PAGly) alter intracellular Ca2+ signaling in isolated mouse ventricular myocytes?
Does phenylacetylglycine (PAGly) alter intracellular Ca2+ signaling in isolated mouse ventricular myocytes?
The gut microbiota metabolite PAGly mildly stimulates cardiac Ca2+ transients by activating beta-adrenergic receptors, but acts as a competitive antagonist to blunt the stronger inotropic effects of sympathetic stimulation, providing a cellular mechanism for its association with cardiovascular disease.
May blunt sympathetic drive in myocytes; hypothesis-generating for microbiota effects on human cardiac adrenergic signaling.
Phenylacetylglutamine (PAGln) and phenylacetylglycine (PAGly) are small molecules derived from the metabolism of phenylalanine by gut microbiota. Elevated levels of PAGln and PAGly in serum have been associated with increased risks for cardiovascular diseases. It has been suggested that PAGln and PAGly reduce cardiac contraction by blunting the adrenergic response during sympathetic stimulation. However, little is known about whether the effect of PAGln and PAGly on the heart function is associated with an alteration of intracellular Ca
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Bovo et al. (2026) studied this question. Phenylacetylglycine activates adrenergic signaling in ventricular myocytes less efficiently than selective agonists, potentially blunting the stimulatory effect of sympathetic stimulation.
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