ReviewAmerican journal of physiology. Heart and circulatory physiology2021
Cardiac α1A-adrenergic receptors: emerging protective roles in cardiovascular diseases.
Review in American journal of physiology. Heart and circulatory physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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
37 citing papers in PubMed, 61 citations in OpenAlex.
- Does preoperative silodosin administration facilitate ureteral dilatation during flexible ureterorenoscopy? A randomized clinical trial.International urology and nephrology · 2024Trial
- ASIV Attenuates Cisplatin-Induced Proximal Tubular Injury by Enhancing Mitochondrial Biogenesis and Mitophagy Through the ADRA1A/AMPK/FOXO3A Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Adrenergic Pathways Mediate Circadian IOP Rhythm in Rats.Investigative ophthalmology & visual science · 2026Article
- The nuclear receptor ROR-alpha is a putative novel myogenic regulator of the cardiomyocyte transcriptome, including the alpha-1A adrenergic receptor.American journal of physiology. Heart and circulatory physiology · 2026Article
- Midodrine to facilitate cardioprotective therapy in hypotensive HER2-positive breast cancer patients with cancer-therapy-related cardiac dysfunction-multicenter case experience.Cardio-oncology (London, England) · 2026Article
- Chronic therapy with α1A-adrenergic agonist reverses RV failure and mitochondrial dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Midodrine to Facilitate Guideline-Directed Medical Therapy in Heart Failure with Reduced Ejection Fraction: A Promising Breakthrough or Just a False Hope?American journal of cardiovascular drugs : drugs, devices, and other interventions · 2026Review
- Systematic evaluation of Tox21 compounds that target β-adrenergic receptors and their role in cardiotoxicity.Toxicology and applied pharmacology · 2025Article
- The perinatal llama immersed in the thin oxygen of the Andean Altiplano.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Role of membrane microdomains in cardiac protection: strategies for diabetic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2025Review
- Novel insights into post-myocardial infarction cardiac remodeling through algorithmic detection of cell-type composition shifts.PLoS genetics · 2025Article
- A gatekeeper sympathetic control of lacrimal tear secretion and dry eye onset through the NA-Adra1a-Ucp2 pathway.Nature communications · 2025Article
- Co-administration of isoprenaline and phenylephrine induced a new HFrEF mouse model through activation of both SNS and RAAS.Frontiers in cardiovascular medicine · 2025Article
- From radiolabeling to receptor quantification: preclinical assessment of [Frontiers in pharmacology · 2025Article
- The Role of αBulletin of experimental biology and medicine · 2025Article
- Developmental Changes in the Excitation-Contraction Mechanisms of the Ventricular Myocardium and Their Sympathetic Regulation in Small Experimental Animals.Journal of cardiovascular development and disease · 2024Review
- Protein glycosylation in cardiovascular health and disease.Nature reviews. Cardiology · 2024Review
- The alpha-1A adrenergic receptor regulates mitochondrial oxidative metabolism in the mouse heart.Journal of molecular and cellular cardiology · 2024Article
- Adrenoceptors in the Eye - Physiological and Pathophysiological Relevance.Handbook of experimental pharmacology · 2024Review
- Cardiomyocyte Alpha-1A Adrenergic Receptors Mitigate Postinfarct Remodeling and Mortality by Constraining Necroptosis.JACC. Basic to translational science · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
α1-Adrenergic receptors (ARs) are catecholamine-activated G protein-coupled receptors (GPCRs) that are expressed in mouse and human myocardium and vasculature, and play essential roles in the regulation of cardiovascular physiology. Though α1-ARs are less abundant in the heart than β1-ARs, activation of cardiac α1-ARs results in important biologic processes such as hypertrophy, positive inotropy, ischemic preconditioning, and protection from cell death. Data from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) indicate that nonselectively blocking α1-ARs is associated with a twofold increase in adverse cardiac events, including heart failure and angina, suggesting that α1-AR activation might also be cardioprotective in humans. Mounting evidence implicates the α1A-AR subtype in these adaptive effects, including prevention and reversal of heart failure in animal models by α1A agonists. In this review, we summarize recent advances in our understanding of cardiac α1A-ARs.
Indexed as
Identifiers
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.