ArticleJournal of the American Heart Association2016
Genetic Abrogation of Adenosine A3 Receptor Prevents Uninephrectomy and High Salt-Induced Hypertension.
Article in Journal of the American Heart Association, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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22 citing papers in PubMed, 34 citations in OpenAlex.
- Stellate ganglion irradiation alleviates airway inflammation in asthmatic mice via activating SIRT1 signaling pathway.Scientific reports · 2025Article
- A novel model of cardiovascular-kidney-metabolic syndrome combining unilateral nephrectomy and high-salt-sugar-fat diet in mice.Lab animal · 2024Article
- Adenosine AInternational journal of molecular sciences · 2024Review
- Purinergic Signaling and its Role in the Stem Cell Differentiation.Mini reviews in medicinal chemistry · 2024Review
- Purinoceptor: a novel target for hypertension.Purinergic signalling · 2023Review
- Adenosine receptors as emerging therapeutic targets for diabetic kidney disease.Kidney research and clinical practice · 2022Article
- Hyperhomocysteinemia and Cardiovascular Disease: Is the Adenosinergic System the Missing Link?International journal of molecular sciences · 2021Review
- Effects of Caffeine on Brown Adipose Tissue Thermogenesis and Metabolic Homeostasis: A Review.Frontiers in neuroscience · 2021Review
- Consumption of salt leads to ameliorate symptoms of metabolic disorder and change of gut microbiota.European journal of nutrition · 2020Article
- Identification and characterization of adipose surface epitopes.The Biochemical journal · 2020Review
- Review
- Ability of CP-532,903 to protect mouse hearts from ischemia/reperfusion injury is dependent on expression of ABiochemical pharmacology · 2019Article
- Genetic ablation of adenosine receptor A3 results in articular cartilage degeneration.Journal of molecular medicine (Berlin, Germany) · 2018Article
- The Role of Adenosine Receptor Activation in Attenuating Cartilaginous Inflammation.Inflammation · 2018Review
- Mechanisms in hypertension and target organ damage: Is the role of the thymus key? (Review).International journal of molecular medicine · 2018Review
- Adenosine Receptor-Mediated Cardioprotection-Current Limitations and Future Directions.Frontiers in pharmacology · 2018Article
- Article
- Dietary nitrate attenuates renal ischemia-reperfusion injuries by modulation of immune responses and reduction of oxidative stress.Redox biology · 2017Article
- Pathological overproduction: the bad side of adenosine.British journal of pharmacology · 2017Review
- Targeting Adenosine Receptors for the Treatment of Cardiac Fibrosis.Frontiers in pharmacology · 2017Review
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEarly-life reduction in nephron number (uninephrectomy [UNX]) and chronic high salt (HS) intake increase the risk of hypertension and chronic kidney disease. Adenosine signaling via its different receptors has been implicated in modulating renal, cardiovascular, and metabolic functions as well as inflammatory processes; however, the specific role of the A3 receptor in cardiovascular diseases is not clear. In this study, gene-modified mice were used to investigate the hypothesis that lack of A3 signaling prevents the development of hypertension and attenuates renal and cardiovascular injuries following UNX in combination with HS (UNX-HS) in mice. METHODS AND
resultsWild-type (A3 (+/+)) mice subjected to UNX-HS developed hypertension compared with controls (mean arterial pressure 106±3 versus 82±3 mm Hg; P<0.05) and displayed an impaired metabolic phenotype (eg, increased adiposity, reduced glucose tolerance, hyperinsulinemia). These changes were associated with both cardiac hypertrophy and fibrosis together with renal injuries and proteinuria. All of these pathological hallmarks were significantly attenuated in the A3 (-/-) mice. Mechanistically, absence of A3 receptors protected from UNX-HS-associated increase in renal NADPH oxidase activity and Nox2 expression. In addition, circulating cytokines including interleukins 1β, 6, 12, and 10 were increased in A3 (+/+) following UNX-HS, but these cytokines were already elevated in naïve A3 (-/-) mice and did not change following UNX-HS.
conclusionsReduction in nephron number combined with chronic HS intake is associated with oxidative stress, chronic inflammation, and development of hypertension in mice. Absence of adenosine A3 receptor signaling was strongly protective in this novel mouse model of renal and cardiovascular disease.
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