ReviewAmerican journal of physiology. Heart and circulatory physiology2026
Phosphodiesterase 8 regulation of excitation-contraction coupling as a target for cardiovascular disease: is it my turn now?
Review in American journal of physiology. Heart and circulatory physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Heart failure is a major cause of cardiac mortality in the United States and globally. It occurs when the heart cannot pump enough blood to meet the body's needs, often due to stiffness of the heart muscle or dysfunction in its ability to contract. Cardiac remodeling in heart failure is an adaptive response to this impaired function. Among the pathways involved in this adaptation, the sympathetic nervous system, specifically, β-adrenergic receptors (β-ARs), plays a central role. Stimulation of β-ARs enhances cardiac contractility by activating protein kinase A (PKA), a key mediator in downstream signaling that regulates excitation-contraction coupling (ECC) through ECC-related proteins. A-kinase-anchoring proteins (AKAPs) act as scaffolds for PKA, organizing compartmentalized signaling events. Recent studies have highlighted the role of AKAP12 in recruiting phosphodiesterase 8 (PDE8) following β-ARs activation. PDE8 is a cyclic adenosine monophosphate (cAMP)-specific phosphodiesterase that hydrolyzes cAMP, thereby limiting the inotropic responses mediated by β-ARs. Although other PDE isoforms (PDE3, PDE4, and PDE5) have been extensively studied and targeted for therapy in heart failure, PDE8 has received relatively little attention. This review discusses the emerging roles of PDE8 across various physiological systems, with a particular focus on the cardiovascular system and its potential as a therapeutic target.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.