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Keywords = A-kinase-anchoring protein

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28 pages, 3566 KiB  
Review
Role of PDE4 Family in Cardiomyocyte Physiology and Heart Failure
by Ivan Sherstnev, Aleksandra Judina, Giovanni Battista Luciani, Alessandra Ghigo, Emilio Hirsch and Julia Gorelik
Cells 2025, 14(6), 460; https://doi.org/10.3390/cells14060460 - 20 Mar 2025
Viewed by 1507
Abstract
Phosphodiesterase 4 (PDE4) is a key regulator of cyclic adenosine monophosphate (cAMP) signalling in cardiomyocytes, controlling contractility, calcium handling, and hypertrophic responses. PDE4 provides spatial and temporal precision to cAMP signalling, particularly under β-adrenergic stimulation, through its compartmentalised activity in subcellular nanodomains, including [...] Read more.
Phosphodiesterase 4 (PDE4) is a key regulator of cyclic adenosine monophosphate (cAMP) signalling in cardiomyocytes, controlling contractility, calcium handling, and hypertrophic responses. PDE4 provides spatial and temporal precision to cAMP signalling, particularly under β-adrenergic stimulation, through its compartmentalised activity in subcellular nanodomains, including the sarcoplasmic reticulum, plasma membrane and nuclear envelope. This review highlights the cardiac PDE4 isoforms PDE4A, PDE4B and PDE4D, focusing on their distinct localisation and contributions to cardiac physiology and pathophysiology, particularly in heart failure and arrhythmias. Although PDE4 plays a smaller role in overall cAMP hydrolysis in human hearts than in rodents, its compartmentalised function remains critical. Recent therapeutic advances have shifted from pan-PDE4 inhibitors to isoform-specific approaches to enhance efficacy while minimising systemic toxicity. We discuss the potential of selective PDE4 modulators, gene therapies and combination strategies in restoring cAMP compartmentation and preventing maladaptive cardiac remodelling. By integrating rodent and human studies, this review underscores the translational challenges and therapeutic opportunities surrounding PDE4, positioning it as both a key regulator of cardiac signalling and a promising target for heart failure therapies. Full article
(This article belongs to the Special Issue Phosphodiesterases (PDEs): Therapeutic Targets in Human Health and Disease)
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14 pages, 3092 KiB  
Article
InDel and CNV within the AKAP13 Gene Revealing Strong Associations with Growth Traits in Goat
by Xiaoyue Song, Yangyang Bai, Rongrong Yuan, Haijing Zhu, Xianyong Lan and Lei Qu
Animals 2023, 13(17), 2746; https://doi.org/10.3390/ani13172746 - 29 Aug 2023
Cited by 3 | Viewed by 1721
Abstract
A-kinase-anchoring protein 13 (AKAP13) is a member of the AKAP protein family that has been found to be associated with bone formation. Thus, we investigated the AKAP13 gene as a potential candidate gene for molecular-marker-assisted selection (MAS) in breeding. Our aim [...] Read more.
A-kinase-anchoring protein 13 (AKAP13) is a member of the AKAP protein family that has been found to be associated with bone formation. Thus, we investigated the AKAP13 gene as a potential candidate gene for molecular-marker-assisted selection (MAS) in breeding. Our aim was to explore genetic variations (InDel and CNV) within the AKAP13 gene of Shaanbei white cashmere (SBWC) goats and analyze their relationship with growth traits. Ultimately, we identified three InDel loci (16-bp deletion, 15-bp insertion, and 25-bp deletion) and three CNVs, and the 16-bp and 15-bp loci were significantly associated with goat body length (p < 0.05). Both the 16-bp deletion variant and the 15-bp insertion variant facilitated an increase in body length in goats. In addition to this, there was a certain superposition effect between 16-bp and 15-bp loci, although there was no linkage. Additionally, the CNV1 locus was significantly correlated with body height and body length of goats (p < 0.05), and CNV2 was significantly correlated with chest depth, chest circumference, and cannon circumference of goats (p < 0.05). Individuals with gain type showed excellent growth performance. In conclusion, the InDel and CNV loci that we have identified could possibly serve as effective molecular markers in goat breeding, which is very essential for improving efficiency and success of breeding. Moreover, our findings provide a new avenue for further research into the function of the AKAP13 gene. Full article
(This article belongs to the Section Animal Genetics and Genomics)
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24 pages, 4935 KiB  
Article
A-Kinase Anchoring Protein 2 Promotes Protection against Myocardial Infarction
by Darko Maric, Aleksandra Paterek, Marion Delaunay, Irene Pérez López, Miroslav Arambasic and Dario Diviani
Cells 2021, 10(11), 2861; https://doi.org/10.3390/cells10112861 - 23 Oct 2021
Cited by 17 | Viewed by 4509
Abstract
Myocardial infarction (MI) is a leading cause of maladaptive cardiac remodeling and heart failure. In the damaged heart, loss of function is mainly due to cardiomyocyte death and remodeling of the cardiac tissue. The current study shows that A-kinase anchoring protein 2 (AKAP2) [...] Read more.
Myocardial infarction (MI) is a leading cause of maladaptive cardiac remodeling and heart failure. In the damaged heart, loss of function is mainly due to cardiomyocyte death and remodeling of the cardiac tissue. The current study shows that A-kinase anchoring protein 2 (AKAP2) orchestrates cellular processes favoring cardioprotection in infarcted hearts. Induction of AKAP2 knockout (KO) in cardiomyocytes of adult mice increases infarct size and exacerbates cardiac dysfunction after MI, as visualized by increased left ventricular dilation and reduced fractional shortening and ejection fraction. In cardiomyocytes, AKAP2 forms a signaling complex with PKA and the steroid receptor co-activator 3 (Src3). Upon activation of cAMP signaling, the AKAP2/PKA/Src3 complex favors PKA-mediated phosphorylation and activation of estrogen receptor α (ERα). This results in the upregulation of ER-dependent genes involved in protection against apoptosis and angiogenesis, including Bcl2 and the vascular endothelial growth factor a (VEGFa). In line with these findings, cardiomyocyte-specific AKAP2 KO reduces Bcl2 and VEGFa expression, increases myocardial apoptosis and impairs the formation of new blood vessels in infarcted hearts. Collectively, our findings suggest that AKAP2 organizes a transcriptional complex that mediates pro-angiogenic and anti-apoptotic responses that protect infarcted hearts. Full article
(This article belongs to the Special Issue Scaffold Proteins in Health, Disease, and Therapy)
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