Popeye proteins: muscle for the aging sinus node
Bastiaan J. Boukens, Vincent M. Christoffels
Bastiaan J. Boukens, Vincent M. Christoffels
Published February 22, 2012
Citation Information: J Clin Invest. 2012;122(3):810-813. https://doi.org/10.1172/JCI62588.
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Commentary

Popeye proteins: muscle for the aging sinus node

Abstract

The electrical impulses that dictate the rhythm of the heartbeat in normal situations and during exercise or stress are initiated by a small number of sinus node pacemaker cells. Senescence and dysfunction of the sinus node affects many people later in life, causing physiologically inappropriate heart rates, but the underlying mechanisms are not well understood. In this issue of the JCI, Froese and colleagues show that deficiency in either Popeye domain containing 1 (Popdc1) or Popdc2 leads to sinus node dysfunction under stressed conditions in aged mice. The mechanism reported to underlie the effects of Popdc1/2 deficiency in mice may cause the stress-induced sinus node dysfunction found in many aged individuals and may point to new strategies for therapeutic intervention.

Authors

Bastiaan J. Boukens, Vincent M. Christoffels

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Figure 2

Mechanism of modifying TREK-1 current in rest and during stress.

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Mechanism of modifying TREK-1 current in rest and during stress. (A) Mec...
(A) Mechanism by which Popdc1 and Popdc2 induce a TREK-1 outward current in resting conditions, as suggested by the work of Froese and colleagues (8). Note that we believe it is possible that Popdc1 and Popdc2 also interact with Scn5a or Ankyrin-B. (B) Increased levels of cAMP induced by β-adrenergic receptor stimulation cause Popdc1 or Popdc2 to release TREK-1, resulting in inhibition of the TREK-1 outward current. This mechanism is absent in mice mutant for either Popdc1 or Popdc2, and therefore TREK-1 current is chronically reduced.