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Cells
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Molecular Insights into cAMP/PKA Pathway Regulation in Health and Disease
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Molecular Insights into cAMP/PKA Pathway Regulation in Health and Disease

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 30 November 2026 | Viewed by 2795

Special Issue Editors

Dr. Elie Seaayfan

E-Mail Website
Guest Editor
Department of Pediatrics, University Hospital Giessen and Marburg, Philipps University Marburg, 35043 Marburg, Germany
Interests: cellular stress; cAMP/PKA signaling pathway; protein trafficking; ER stress; salt transporters; Bartter syndrome; cancer biology; protein–protein interactions; post-translation modifications (PTMs); ubiquitination; protein degradation; autophagy; hypoxia
Prof. Dr. Martin Kömhoff

E-Mail Website
Guest Editor
Department of Pediatrics, University Hospital Giessen and Marburg, Philipps University Marburg, 35043 Marburg, Germany
Interests: cellular stress; cAMP/PKA signaling pathway; protein trafficking; ER stress; salt transporters; Bartter syndrome; cancer biology; protein–protein interactions; renal physiology; macula densa; autophagy; hypoxia

Special Issue Information

Dear Colleagues,

This Special Issue, “Molecular Insights into cAMP/PKA Pathway Regulation in Health and Disease”, aims to explore the intricate molecular mechanisms that regulate the cyclic AMP (cAMP)/Protein Kinase A (PKA) signaling pathway and its impact on cellular function in both normal physiology and disease states. The cAMP/PKA pathway is a critical signaling cascade involved in numerous biological processes, including metabolism, cellular stress responses, gene regulation, and neurotransmission. Dysregulation of this pathway has been implicated in a range of diseases, including metabolic disorders, cardiovascular diseases, cancer, and neurodegenerative conditions.

The contributions in this issue will address various aspects of cAMP/PKA signaling, including its role in cellular homeostasis, cross-talk with other signaling pathways, molecular regulators, and therapeutic interventions targeting pathway dysregulation. We invite original research articles and reviews that provide novel insights into this vital signaling axis, with a particular focus on its implications in disease pathology and potential therapeutic strategies.

Dr. Elie Seaayfan
Prof. Dr. Martin Kömhoff
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cAMP/PKA signaling
  • protein kinase A (PKA)
  • cyclic AMP
  • EPAC
  • signal transduction
  • cellular homeostasis
  • metabolic regulation
  • disease mechanisms
  • molecular signaling
  • therapeutic targets
  • cross-talk in signaling pathways
  • protein–protein interactions
  • post-translational modifications
  • pharmacological interventions

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Published Papers (2 papers)

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Research

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20 pages, 3775 KB  
Article
Sustained CREB Phosphorylation Is Associated with Neuritogenic Prostanoid Signaling in NSC-34 Cells
by Koume Nagayama, Hiroshi Nango, Komugi Tsuruta, Hiroko Miyagishi and Yasuhiro Kosuge
Cells 2026, 15(11), 1004; https://doi.org/10.3390/cells15111004 - 29 May 2026
Abstract
Neuritogenesis is essential for neuronal development and circuit formation. Although cAMP signaling downstream of Gs-coupled receptors is considered pro-neuritogenic, activation of these Gs-coupled receptors can produce divergent cellular outcomes. We previously showed that prostaglandin E2 (PGE2) induces neurite outgrowth in [...] Read more.
Neuritogenesis is essential for neuronal development and circuit formation. Although cAMP signaling downstream of Gs-coupled receptors is considered pro-neuritogenic, activation of these Gs-coupled receptors can produce divergent cellular outcomes. We previously showed that prostaglandin E2 (PGE2) induces neurite outgrowth in NSC-34 motor neuron-like cells predominantly through Gs-coupled E-prostanoid receptor 2 (EP2) signaling. The I-prostanoid receptor (IP) is also Gs-coupled, but whether its ligand PGI2 elicits neuritogenesis remains unclear. Here, we compare the neuritogenic and signaling responses to PGE2 and PGI2 in NSC-34 cells. PGE2 and the EP2 agonist butaprost increased the proportion of neurite-bearing cells, whereas PGI2 and the IP agonist beraprost had no effect. PGI2 and PGE2 induced comparable cAMP accumulation and protein kinase A substrate phosphorylation, and elicited peak cAMP response element binding protein (CREB) phosphorylation at 1 h. However, only PGE2 maintained significant CREB phosphorylation at 3–6 h. RNA sequencing at 4 h revealed broadly concordant transcriptional responses, while direct comparison identified Fst as the only gene expressed at higher levels under PGE2 than under PGI2. These findings suggest that the temporal profile of CREB phosphorylation, rather than the magnitude of early cAMP-PKA signaling, may be associated with differences in neuritogenic outcomes of Gs-coupled prostanoid signaling. Full article
(This article belongs to the Special Issue Molecular Insights into cAMP/PKA Pathway Regulation in Health and Disease)

Review

Jump to: Research

24 pages, 1810 KB  
Review
Protein Kinase A Signaling in Cortisol Production and Adrenal Cushing’s Syndrome
by Abhishek Kumar, Abhimanyu Sharma and Mitchell H. Omar
Cells 2026, 15(1), 63; https://doi.org/10.3390/cells15010063 - 29 Dec 2025
Viewed by 1572
Abstract
The adenosine 3′,5′-cyclic monophosphate–protein kinase A (cAMP-PKA) signaling pathway is highly utilized in human physiology. It is a crucial component of development and is vital to cellular function in nearly all tissues. Indeed, genetic mutations to cAMP-PKA machinery are found in many pathologies, [...] Read more.
The adenosine 3′,5′-cyclic monophosphate–protein kinase A (cAMP-PKA) signaling pathway is highly utilized in human physiology. It is a crucial component of development and is vital to cellular function in nearly all tissues. Indeed, genetic mutations to cAMP-PKA machinery are found in many pathologies, including multiple cancers, cardiac myxoma, neurodevelopmental disorders, and hypercortisolism. Cyclic AMP and PKA were first identified as vital components in cortisol synthesis over 50 years ago, yet the cellular mechanisms connecting PKA to cortisol production are still not well understood. This article will review evidence for PKA’s roles in adrenal gland zona fasciculata steroidogenesis and consider recent studies of the stress hormone disease adrenal Cushing’s syndrome to synthesize a current model for cAMP-PKA actions in cortisol production. Full article
(This article belongs to the Special Issue Molecular Insights into cAMP/PKA Pathway Regulation in Health and Disease)
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