ReviewAntioxidants & redox signaling2014
Abnormal Ca(2+) cycling in failing ventricular myocytes: role of NOS1-mediated nitroso-redox balance.
Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 17 citations in OpenAlex.
- Involvement of Oxidative Stress in the Development of Subcellular Defects and Heart Disease.Biomedicines · 2022Review
- Oxidative Stress as A Mechanism for Functional Alterations in Cardiac Hypertrophy and Heart Failure.Antioxidants (Basel, Switzerland) · 2021Review
- Reversal of right ventricular failure by chronic αAmerican journal of physiology. Heart and circulatory physiology · 2019Article
- Atrial Infarction-Induced Spontaneous Focal Discharges and Atrial Fibrillation in Sheep: Role of Dantrolene-Sensitive Aberrant Ryanodine Receptor Calcium Release.Circulation. Arrhythmia and electrophysiology · 2018Article
- Article
- Sex Differences in Metabolic Cardiomyopathy.Cardiovascular research · 2017Article
- Ischemic postconditioning protects the heart against ischemia-reperfusion injury via neuronal nitric oxide synthase in the sarcoplasmic reticulum and mitochondria.Cell death & disease · 2016Article
- Insulin-like growth factor 1 prevents diastolic and systolic dysfunction associated with cardiomyopathy and preserves adrenergic sensitivity.Acta physiologica (Oxford, England) · 2016Article
- Chronic Contractile Dysfunction without Hypertrophy Does Not Provoke a Compensatory Transcriptional Response in Mouse Hearts.PloS one · 2016Article
- Novel Perspectives in Redox Biology and Pathophysiology of Failing Myocytes: Modulation of the Intramyocardial Redox Milieu for Therapeutic Interventions-A Review Article from the Working Group of Cardiac Cell Biology, Italian Society of Cardiology.Oxidative medicine and cellular longevity · 2016Review
- Obligatory role of neuronal nitric oxide synthase in the heart's antioxidant adaptation with exercise.Journal of molecular and cellular cardiology · 2015Article
- Defining the role of oxidative stress in atrial fibrillation and diabetes.Journal of cardiovascular electrophysiology · 2015Article
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 2 institutions in 1 country.
Funding
Abstract
significanceHeart failure (HF) results from poor heart function and is the leading cause of death in Western society. Abnormalities of Ca(2+) handling at the level of the ventricular myocyte are largely responsible for much of the poor heart function. RECENT ADVANCES: Although studies have unraveled numerous mechanisms for the abnormal Ca(2+) handling, investigations over the past decade have indicated that much of the contractile dysfunction and adverse remodeling that occurs in HF involves oxidative stress. CRITICAL ISSUES: Regrettably, antioxidant therapy has been an immense disappointment in clinical trials. Thus, redox signaling is being reassessed to elucidate why antioxidants failed to treat HF. FUTURE DIRECTIONS: A recently identified aspect of redox signaling (specifically the superoxide anion radical) is its interaction with nitric oxide, known as the nitroso-redox balance. There is a large nitroso-redox imbalance with HF, and we suggest that correcting this imbalance may be able to restore myocyte contraction and improve heart function.
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.