ReviewFrontiers in physiology2013
Physiology and pharmacology of the cardiovascular adrenergic system.
Review in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 18 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
18 citing papers in PubMed, 42 citations in OpenAlex.
- Status of βReviews in cardiovascular medicine · 2023Review
- β2-Adrenergic Receptor Mediated Inhibition of T Cell Function and Its Implications for CAR-T Cell Therapy.International journal of molecular sciences · 2023Review
- Cardiac PDGFRαFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Beta-Blocker Use in Older Hospitalized Patients Affected by Heart Failure and Chronic Obstructive Pulmonary Disease: An Italian Survey From the REPOSI Register.Frontiers in cardiovascular medicine · 2022Article
- Catestatin reverses the hypertrophic effects of norepinephrine in H9c2 cardiac myoblasts by modulating the adrenergic signaling.Molecular and cellular biochemistry · 2020Article
- Beta-blocker choice and exchangeability in patients with heart failure and chronic obstructive pulmonary disease: an Italian register-based cohort study.Scientific reports · 2019Article
- Deficiency of NOD1 Improves the β-Adrenergic Modulation of CaFrontiers in physiology · 2018Article
- The natural history of takotsubo syndrome: a two-year follow-up study with myocardial sympathetic and perfusion G-SPECT imaging.European journal of nuclear medicine and molecular imaging · 2017Article
- Emerging role of hydrogen sulfide-microRNA crosstalk in cardiovascular diseases.American journal of physiology. Heart and circulatory physiology · 2016Review
- The influence of inhaled multi-walled carbon nanotubes on the autonomic nervous system.Particle and fibre toxicology · 2016Article
- Semaphorin 3A attenuates cardiac autonomic disorders and reduces inducible ventricular arrhythmias in rats with experimental myocardial infarction.BMC cardiovascular disorders · 2016Article
- Adrenal G protein-coupled receptor kinase-2 in regulation of sympathetic nervous system activity in heart failure.World journal of cardiology · 2015Review
- Renal impairment and worsening of renal function in acute heart failure: can new therapies help? The potential role of serelaxin.Clinical research in cardiology : official journal of the German Cardiac Society · 2015Review
- Cardiac Dysfunction Induced by Obesity Is Not Related to β-Adrenergic System Impairment at the Receptor-Signalling Pathway.PloS one · 2015Article
- Adrenal adrenoceptors in heart failure.Frontiers in physiology · 2014Review
- Regulatory SNPs and transcriptional factor binding sites in ADRBK1, AKT3, ATF3, DIO2, TBXA2R and VEGFA.Transcription · 2014Review
- The adrenergic system in cardiovascular pathophysiology: a translational science point of view.Frontiers in physiology · 2014Article
- βArrestins in cardiac G protein-coupled receptor signaling and function: partners in crime or "good cop, bad cop"?International journal of molecular sciences · 2013Review
Corrections and comments
- Retraction · 2015-11-27Concerns/Issues about Authorship/Affiliation · Duplication of/in Article · Euphemisms for Plagiarism ·
- Retracted
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure (HF), the leading cause of death in the western world, ensues in response to cardiac injury or insult and represents the inability of the heart to adequately pump blood and maintain tissue perfusion. It is characterized by complex interactions of several neurohormonal mechanisms that get activated in the syndrome in order to try and sustain cardiac output in the face of decompensating function. The most prominent among these neurohormonal mechanisms is the adrenergic (or sympathetic) nervous system (ANS), whose activity and outflow are greatly elevated in HF. Acutely, provided that the heart still works properly, this activation of the ANS will promptly restore cardiac function according to the fundamental Frank-Starling law of cardiac function. However, if the cardiac insult persists over time, this law no longer applies and ANS will not be able to sustain cardiac function. This is called decompensated HF, and the hyperactive ANS will continue to "push" the heart to work at a level much higher than the cardiac muscle can handle. From that point on, ANS hyperactivity becomes a major problem in HF, conferring significant toxicity to the failing heart and markedly increasing its morbidity and mortality. The present review discusses the role of the ANS in cardiac physiology and in HF pathophysiology, the mechanisms of regulation of ANS activity and how they go awry in chronic HF, and, finally, the molecular alterations in heart physiology that occur in HF along with their pharmacological and therapeutic implications for the failing heart.
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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.