Adenosine and Adenosine Receptors in Human Disease

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

Deadline for manuscript submissions: closed (20 December 2023) | Viewed by 3623

Special Issue Editor


E-Mail Website1 Website2
Guest Editor
1. Laboratory of Biochemistry, Timone University Hospital, APHM, 13005 Marseille, France
2. Center for CardioVascular and Nutrition Research (C2VN), INSERM, INRAE, Aix-Marseille University, Marseille, France
Interests: adenosinergic system; cardiovascular diseases; cardiac arrythmia; cell signaling transduction
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Special Issue Information

Dear Colleagues,

Since the identification of adenosine in 1929 and the concept of extracellular purinergic signaling being introduced in 1972, adenosine and its four G-protein-coupled receptors have been extensively studied, and there is a growing understanding of the involvement of the adenosinergic system in human diseases. Due to the wide distribution of the adenosine receptors throughout the human body, adenosine has emerged as an important signaling molecule with major and pleiotropic effects in the cardiovascular, central nervous and immune systems. Since adenosine is increased by hypoxia, ischemia or inflammation, improved knowledge of adenosinergic system signaling in human diseases could offer new opportunities in prognosis, diagnosis or therapeutic strategies for cardiovascular diseases, cancer, neurodegenerative and metabolic disorders.

The aim of this Special Issue of Cells, entitled “Adenosine and Adenosine Receptors in Human Disease”, is to provide an overview of the state of the art and to promote new insights into adenosine and adenosine receptors’ involvement in cancer, cardiovascular diseases, neurodegenerative and metabolic disorders. Both original research and review articles consistent with this research topic will be considered for publication.

We look forward to your contributions.

Dr. Julien Fromonot
Guest Editor

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Keywords

  • adenosine
  • adenosine receptors
  • cardiovascular diseases
  • cancer
  • neurodegenerative disorders
  • metabolic disorders
  • hypoxia
  • inflammation
  • ischemia
  • immune system

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Published Papers (2 papers)

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Research

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15 pages, 1812 KiB  
Article
Low Density Lipoprotein Cholesterol Decreases the Expression of Adenosine A2A Receptor and Lipid Rafts-Protein Flotillin-1: Insights on Cardiovascular Risk of Hypercholesterolemia
by Marie-Charlotte Chaptal, Marie Maraninchi, Giorgia Musto, Julien Mancini, Hedi Chtioui, Janine Dupont-Roussel, Marion Marlinge, Julien Fromonot, Nathalie Lalevee, Florian Mourre, Sophie Beliard, Régis Guieu, René Valero and Giovanna Mottola
Cells 2024, 13(6), 488; https://doi.org/10.3390/cells13060488 - 11 Mar 2024
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Abstract
High blood levels of low-density lipoprotein (LDL)-cholesterol (LDL-C) are associated with atherosclerosis, mainly by promoting foam cell accumulation in vessels. As cholesterol is an essential component of cell plasma membranes and a regulator of several signaling pathways, LDL-C excess may have wider cardiovascular [...] Read more.
High blood levels of low-density lipoprotein (LDL)-cholesterol (LDL-C) are associated with atherosclerosis, mainly by promoting foam cell accumulation in vessels. As cholesterol is an essential component of cell plasma membranes and a regulator of several signaling pathways, LDL-C excess may have wider cardiovascular toxicity. We examined, in untreated hypercholesterolemia (HC) patients, selected regardless of the cause of LDL-C accumulation, and in healthy participants (HP), the expression of the adenosine A2A receptor (A2AR), an anti-inflammatory and vasodilatory protein with cholesterol-dependent modulation, and Flotillin-1, protein marker of cholesterol-enriched plasma membrane domains. Blood cardiovascular risk and inflammatory biomarkers were measured. A2AR and Flotillin-1 expression in peripheral blood mononuclear cells (PBMC) was lower in patients compared to HP and negatively correlated to LDL-C blood levels. No other differences were observed between the two groups apart from transferrin and ferritin concentrations. A2AR and Flotillin-1 proteins levels were positively correlated in the whole study population. Incubation of HP PBMCs with LDL-C caused a similar reduction in A2AR and Flotillin-1 expression. We suggest that LDL-C affects A2AR expression by impacting cholesterol-enriched membrane microdomains. Our results provide new insights into the molecular mechanisms underlying cholesterol toxicity, and may have important clinical implication for assessment and treatment of cardiovascular risk in HC. Full article
(This article belongs to the Special Issue Adenosine and Adenosine Receptors in Human Disease)
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Review

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13 pages, 8233 KiB  
Review
Adenosinergic System and Neuroendocrine Syncope: What Is the Link?
by Régis Guieu, Julien Fromonot, Giovanna Mottola, Baptiste Maille, Marion Marlinge, Antonella Groppelli, Samantha Conte, Yassina Bechah, Nathalie Lalevee, Pierre Michelet, Mohamed Hamdan, Michele Brignole and Jean Claude Deharo
Cells 2023, 12(16), 2027; https://doi.org/10.3390/cells12162027 - 8 Aug 2023
Cited by 2 | Viewed by 1621
Abstract
Although very common, the precise mechanisms that explain the symptomatology of neuroendocrine syncope (NES) remain poorly understood. This disease, which can be very incapacitating, manifests itself as a drop in blood pressure secondary to vasodilation and/or extreme slowing of heart rate. As studies [...] Read more.
Although very common, the precise mechanisms that explain the symptomatology of neuroendocrine syncope (NES) remain poorly understood. This disease, which can be very incapacitating, manifests itself as a drop in blood pressure secondary to vasodilation and/or extreme slowing of heart rate. As studies continue, the involvement of the adenosinergic system is becoming increasingly evident. Adenosine, which is an ATP derivative, may be involved in a large number of cases. Adenosine acts on G protein-coupled receptors with seven transmembrane domains. A1 and A2A adenosine receptor dysfunction seem to be particularly implicated since the activation leads to severe bradycardia or vasodilation, respectively, two cardinal symptoms of NES. This mini-review aims to shed light on the links between dysfunction of the adenosinergic system and NHS. In particular, signal transduction pathways through the modulation of cAMP production and ion channels in relation to effects on the cardiovascular system are addressed. A better understanding of these mechanisms could guide the pharmacological development of new therapeutic approaches. Full article
(This article belongs to the Special Issue Adenosine and Adenosine Receptors in Human Disease)
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