ReviewJournal of cardiovascular pharmacology2015
AT2 receptor activities and pathophysiological implications.
Review in Journal of cardiovascular pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 2 syntheses or guidelines pooled it, 116 citations in OpenAlex.
- Pooled it
- Severe acute respiratory syndrome coronavirus 2 and renin-angiotensin system blockers: A review and pooled analysis.Archives of cardiovascular diseases · 2020Pooled it
- Protective Arm of Renin-Angiotensin System: Evidence of Nephroprotective Effects Against Acute Kidney Injury.Acta physiologica (Oxford, England) · 2026Review
- Combined Apocynin and Novokinin Treatment Attenuates Renal Damage and Reduces KIM-1 Expression in a Model of Ischemic AKI.International journal of molecular sciences · 2026Article
- Epicardial adipose tissue as a metabolically active visceral fat depot: an emerging target in cardiovascular disease.Frontiers in cardiovascular medicine · 2026Review
- Angiotensin II type 1 and type 2 receptors modulate TWIK1 channel expression and pain sensitivity in a rat model of neuropathic pain.Frontiers in pharmacology · 2026Article
- Dietary Flavonoids as Cross-System Modulators of Hypertension and Intestinal Permeability.Molecules (Basel, Switzerland) · 2025Review
- Renoprotective effects of compound 21 and empagliflozin in L-Name-induced hypertensive rats.BMC urology · 2025Article
- The Renin-Angiotensin-Aldosterone System (RAAS): Beyond Cardiovascular Regulation.Veterinary sciences · 2025Review
- The Balance Between the Natriuretic Peptides and the Renin-Angiotensin-Aldosterone System in the Preservation of Ideal Cardiovascular Health.Journal of clinical medicine · 2025Review
- Blood Pressure Management Strategies and Podocyte Health.American journal of hypertension · 2025Review
- Impact of Renin-Angiotensin-Aldosterone System (RAAS) Gene Polymorphism in Essential Hypertension and Antihypertensive Drug Therapy: A Review.International journal of hypertension · 2025Review
- Vascular involvement in idiopathic pulmonary fibrosis.ERJ open research · 2024Review
- Stimulation of Angiotensin II Receptor Subtype 2 Reduces Preeclampsia-like Symptoms in a Mouse Model of Preeclampsia.Current issues in molecular biology · 2024Article
- The renin-angiotensin-aldosterone system (RAAS) signaling pathways and cancer: foes versus allies.Cancer cell international · 2023Review
- The Renin Angiotensin System as a Therapeutic Target in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Angiotensin II type 1a receptor knockout ameliorates high-fat diet-induced cardiac dysfunction by regulating glucose and lipid metabolism.Acta biochimica et biophysica Sinica · 2023Article
- Androgen Receptor and Cardiovascular Disease: A Potential Risk for the Abuse of Supplements Containing Selective Androgen Receptor Modulators.Nutrients · 2023Review
- Effects of the Oral Angiotensin II Type 2 Receptor Agonist C21 in Sugen-Hypoxia Induced Pulmonary Hypertension in Rats.International journal of molecular sciences · 2023Article
- Dual Blockade of TGF-β Receptor and Endothelin Receptor Synergistically Inhibits Angiotensin II-Induced Myofibroblast Differentiation: Role of ATInternational journal of molecular sciences · 2023Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Although angiotensin II subtype-2 receptor (AT2R) was discovered over 2 decades ago, its contribution to physiology and pathophysiology is not fully elucidated. Current knowledge suggests that under normal physiologic conditions, AT2R counterbalances the effects of angiotensin II subtype-1 receptor (AT1R). A major obstacle for AT2R investigations was the lack of specific agonists. Most of the earlier AT2R studies were performed using the peptidic agonist, CG42112A, or the nonpeptidic antagonist PD123319. CGP42112A is nonspecific for AT2R and in higher concentrations can bind to AT1R. Recently, the development of specific nonpeptidic AT2R agonists boosted the efforts in identifying the therapeutic potentials for AT2R stimulation. Unlike AT1R, AT2R is involved in vasodilation by the release of bradykinin and nitric oxide, anti-inflammation, and healing from injury. Interestingly, the vasodilatory effects of AT2R stimulation were not associated with significant reduction in blood pressure. In the kidney, AT2R stimulation produced natriuresis, increased renal blood flow, and reduced tissue inflammation. In animal studies, enhanced AT2R function led to reduction of cardiac inflammation and fibrosis, and reduced the size of the infarcted area. Similarly, AT2R stimulation demonstrated protective effects in vasculature and brain.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.