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Adenosine Receptors in Health and Disease
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Adenosine Receptors in Health and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 676

Special Issue Editor

Dr. Srdjan Vlajkovic

E-Mail Website
Guest Editor
Department of Physiology and The Eisdell Moore Centre, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag 92019, Auckland 1142, New Zealand
Interests: sensory systems; auditory neuroscience; inner ear diseases; inner ear therapeutics; hearing loss; inflammation; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Adenosine receptors (ARs) are essential in maintaining health, while altered AR signalling contributes to various disease processes. Adenosine acts as a cytoprotective modulator in response to stress and tissue injury, and understanding AR function is crucial for developing targeted therapies for multiple diseases.

AR signalling regulates physiological functions in the nervous, cardiovascular, and immune systems. For example, ARs regulate blood flow by inducing vasodilation, aiding tissue oxygenation, and protecting against ischemic injuries.

Dysregulation of AR signalling can lead to various pathological conditions, such as pain, cancer, neurodegenerative, inflammatory, and autoimmune diseases. In inflammatory conditions, AR modulation can either suppress or exacerbate immune responses. AR malfunction is also associated with neurological disorders such as epilepsy and Parkinson’s disease.

We invite investigators to contribute original research articles and review articles addressing the various roles of AR in physiology and pathophysiology. Please note that pure clinical or model studies are unsuitable for this journal, but clinical submissions with biomolecular studies are welcome.

Dr. Srdjan Vlajkovic
Guest Editor

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 100 words) can be sent to the Editorial Office for announcement on this website.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • adenosine
  • adenosine receptors
  • P1 receptors
  • A1 receptor
  • A2A receptor
  • A2B receptor
  • A3 receptor
  • adenosine deaminase
  • adenosine kinase
  • adenosine transporters
  • adenosine receptor agonists
  • adenosine receptor antagonists
  • caffeine

Published Papers (1 paper)

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Research

19 pages, 1470 KiB  
Article
Adenosine A2A Receptor Blockade Provides More Effective Benefits at the Onset Rather than after Overt Neurodegeneration in a Rat Model of Parkinson’s Disease
by Ana Carla L. Nunes, Marta Carmo, Andrea Behrenswerth, Paula M. Canas, Paula Agostinho and Rodrigo A. Cunha
Int. J. Mol. Sci. 2024, 25(9), 4903; https://doi.org/10.3390/ijms25094903 - 30 Apr 2024
Viewed by 179
Abstract
Adenosine A2A receptor (A2AR) antagonists are the leading nondopaminergic therapy to manage Parkinson’s disease (PD) since they afford both motor benefits and neuroprotection. PD begins with a synaptic dysfunction and damage in the striatum evolving to an overt neuronal damage [...] Read more.
Adenosine A2A receptor (A2AR) antagonists are the leading nondopaminergic therapy to manage Parkinson’s disease (PD) since they afford both motor benefits and neuroprotection. PD begins with a synaptic dysfunction and damage in the striatum evolving to an overt neuronal damage of dopaminergic neurons in the substantia nigra. We tested if A2AR antagonists are equally effective in controlling these two degenerative processes. We used a slow intracerebroventricular infusion of the toxin MPP+ in male rats for 15 days, which caused an initial loss of synaptic markers in the striatum within 10 days, followed by a neuronal loss in the substantia nigra within 30 days. Interestingly, the initial loss of striatal nerve terminals involved a loss of both dopaminergic and glutamatergic synaptic markers, while GABAergic markers were preserved. The daily administration of the A2AR antagonist SCH58261 (0.1 mg/kg, i.p.) in the first 10 days after MPP+ infusion markedly attenuated both the initial loss of striatal synaptic markers and the subsequent loss of nigra dopaminergic neurons. Strikingly, the administration of SCH58261 (0.1 mg/kg, i.p. for 10 days) starting 20 days after MPP+ infusion was less efficacious to attenuate the loss of nigra dopaminergic neurons. This prominent A2AR-mediated control of synaptotoxicity was directly confirmed by showing that the MPTP-induced dysfunction (MTT assay) and damage (lactate dehydrogenase release assay) of striatal synaptosomes were prevented by 50 nM SCH58261. This suggests that A2AR antagonists may be more effective to counteract the onset rather than the evolution of PD pathology. Full article
(This article belongs to the Special Issue Adenosine Receptors in Health and Disease)
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