-
Tytuł:
-
"Adenosine an old player with new possibilities in kidney diseases": Preclinical evidences and clinical perspectives.
-
Autorzy:
-
Pandey S; Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India.
Aggarwal D; Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India.
Gupta K; Department of Pharmacy, Maharishi Markandeshwar University, Mullana, Ambala, Haryana, India.
Kumari A; Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India.
Sen P; Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India.
Singh R; Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India.
Joshi JC; Department of Pharmacology, College of Medicine, University of Illinois at Chicago, USA.
Sharma VV; Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India.
Mehra K; Department of Pharmacy, Maharishi Markandeshwar University, Mullana, Ambala, Haryana, India.
Singh G; Department of Pharmacology, ISF College of Pharmacy, Moga, Punjab, India. Electronic address: .
-
Źródło:
-
Life sciences [Life Sci] 2021 Jan 15; Vol. 265, pp. 118834. Date of Electronic Publication: 2020 Nov 26.
-
Typ publikacji:
-
Journal Article; Review
-
Język:
-
English
-
Imprint Name(s):
-
Publication: <2008->: Amsterdam : Elsevier
Original Publication: Oxford; Elmsford, N. Y. [etc.] Pergamon Press.
-
MeSH Terms:
-
Adenosine/*metabolism
Kidney Diseases/*physiopathology
Receptors, Purinergic P1/*metabolism
Acute Kidney Injury/drug therapy ; Acute Kidney Injury/physiopathology ; Adenosine Kinase/antagonists & inhibitors ; Adenosine Kinase/metabolism ; Animals ; Humans ; Kidney Diseases/drug therapy ; Reperfusion Injury/physiopathology
-
Contributed Indexing:
-
Keywords: AKI; Adenosine receptors; Apoptosis; Inflammation; Ischemia and reperfusion injury; Radio contrast induced renal injury
-
Substance Nomenclature:
-
0 (Receptors, Purinergic P1)
EC 2.7.1.20 (Adenosine Kinase)
K72T3FS567 (Adenosine)
-
Entry Date(s):
-
Date Created: 20201129 Date Completed: 20210114 Latest Revision: 20210114
-
Update Code:
-
20240105
-
DOI:
-
10.1016/j.lfs.2020.118834
-
PMID:
-
33249096
-
Renal injury might originate from multiple factors like ischemia reperfusion (I/R), drug toxicity, cystic fibrosis, radio contrast agent etc. The four adenosine receptor subtypes have been identified and found to show diverse physiological and pathological roles in kidney diseases. The activation of A 1 adenosine receptor (A 1 ) protects against acute kidney injury by improving renal hemodynamic alterations, decreasing tubular necrosis and its inhibition might facilitate removal of toxin or drug metabolite in chronic kidney disease models. Furthermore, recent findings revealed that A 2A receptor subtype activation regulates macrophage phenotype in experimental models of nephritis. Interestingly the emerging role of adenosine kinase inhibitors in kidney diseases has been discussed which act by increasing adenosine availability at target sites and thereby promote A 2A receptor stimulation. In addition, the least explored adenosine receptor subtype A 3 inhibition was observed to exert anti- oxidant, immunosuppressive and anti-fibrotic effects, but more studies are required to confirm its benefits in other renal injury models. The clinical studies targeting A 1 receptor in patients with pre-existing kidney disease have yielded disappointing results, perhaps owing to the origin of unexpected neurological complications during the course of trial. Importantly, conducting well designed clinical trials and testing adenosine modulators with lesser brain penetrability could clear the way for clinical approval of these agents for patients with renal functional impairments.
(Copyright © 2020 Elsevier Inc. All rights reserved.)