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Cells
Special Issues
AMPK: From Mechanisms to New Therapies
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AMPK: From Mechanisms to New Therapies

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

Deadline for manuscript submissions: 15 December 2025 | Viewed by 553

Special Issue Editors

Dr. Roland Abi Nahed

E-Mail Website
Guest Editor
Laboratory of Fundamental and Applied Bioenergetics (LBFA), Université Grenoble Alpes, Grenoble, France
Interests: placenta growth factor; pregnancy toxemia; endoglin
Dr. Farah Diab

E-Mail Website
Guest Editor
Institut National de la Santé et de la Recherche Médicale (INSERM), Maladies Génétiques d'expression Pédiatrique, Sorbonne Université, Paris, France
Interests: autoinflammatory diseases; inflammasomes; developmental disorders; iPSCs; genetics; variants

Special Issue Information

Dear Colleagues,

AMP-activated protein kinase (AMPK) has emerged as a central regulator of cellular energy homeostasis and a key modulator of various physiological and pathological processes. Its role is highly context-dependent, varying with tissue type, metabolic status, and disease condition. Understanding how AMPK functions in different biological systems and how its signaling pathways become dysregulated is essential for developing targeted therapeutic strategies.

This Special Issue will explore the multifaceted roles of AMPK in health and disease. Topics will include its involvement in metabolic disorders such as type 2 diabetes and obesity, where AMPK activation enhances insulin sensitivity and glucose uptake; in cancer, where it influences cell proliferation, metabolism, and the tumor microenvironment; and in reproductive health, particularly placenta-related pathologies and male fertility, where it regulates energy balance, nutrient transport, and sperm function. We will also highlight the role of AMPK in skin health, including aging, inflammation, and barrier dysfunction, and its broader implications in stress responses and cellular adaptation.

We welcome original research articles, reviews, and communications that provide new insights into the regulatory mechanisms, physiological functions, and translational applications of AMPK in health and disease. The aim of this Special Issue is to provide a comprehensive overview of current advances in AMPK biology, from molecular mechanisms and regulatory networks to novel therapeutic strategies.

By submitting to this Special Issue, authors will gain visibility in a community of researchers focused on AMPK. It is a great opportunity to share your latest findings, help shape the future of AMPK research, and connect with others interested in new ideas and discoveries. This issue offers a unique chance to highlight your work, encourage collaborations, and contribute to the link between basic science and clinical applications.

Dr. Roland Abi Nahed
Dr. Farah Diab
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

  • metabolism
  • AMPK
  • cancer
  • biosensors
  • reproduction
  • metabolic disorders
  • therapies

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

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Research

19 pages, 3412 KB  
Article
AICAR Inhibits Insulin-Stimulated Glucose Uptake in 3T3-L1 Adipocytes via an AMPK-Independent, ZMP-Dependent Mechanism
by Yazeed Alshuweishi, Fatmah Binzomah Alghamdi, Kieran Patrick and Ian P. Salt
Cells 2025, 14(22), 1811; https://doi.org/10.3390/cells14221811 - 18 Nov 2025
Viewed by 301
Abstract
AMP-activated protein kinase (AMPK) is activated by reduced cellular energy charge and mimics the action of insulin in muscle by stimulating increased trafficking of GLUT4 to the plasma membrane. In contrast, we have previously reported that short-term activation of AMPK in adipocytes has [...] Read more.
AMP-activated protein kinase (AMPK) is activated by reduced cellular energy charge and mimics the action of insulin in muscle by stimulating increased trafficking of GLUT4 to the plasma membrane. In contrast, we have previously reported that short-term activation of AMPK in adipocytes has no effect on glucose uptake. Whether prolonged AMPK activation influences adipocyte glucose uptake remains poorly characterised. To investigate the effect of sustained AMPK activation on glucose uptake in adipocytes, glucose uptake and insulin signalling were assessed in 3T3-L1 adipocytes stimulated with AICAR and 991, which activate AMPK by different mechanisms, for 24 h. Furthermore, glucose uptake and GLUT4 levels were assessed in adipocytes or adipose tissue from mice lacking AMPKα1 as a model of prolonged AMPK downregulation. AICAR, but not 991, markedly inhibited insulin-stimulated glucose uptake in 3T3-L1 adipocytes. This effect of AICAR was associated with impaired trafficking of GLUT4 to the plasma membrane but did not alter cellular GLUT4 levels or insulin signalling via AKT. The effect of AICAR did, however, require phosphorylation to the nucleotide ZMP and was associated with altered insulin-stimulated MEK1/2-ERK1/2 phosphorylation. Sustained AMPK downregulation had no effect on adipocyte glucose uptake or GLUT4 levels. Taken together, these data demonstrate that sustained changes in AMPK activity do not alter adipocyte glucose uptake. Furthermore, AICAR reduces insulin-stimulated GLUT4 translocation and glucose uptake in adipocytes by a mechanism that is independent of AMPK but requires phosphorylation of AICAR to ZMP. Full article
(This article belongs to the Special Issue AMPK: From Mechanisms to New Therapies)
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