ReviewInternational journal of molecular sciences2013
The NO/ONOO-cycle as the central cause of heart failure.
Review in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 59 citations in OpenAlex.
- The Influence of Basic Therapy and New Drugs on NO-Dependent Mechanisms of Cardiac Destruction in Chronic Heart Failure.Biomedicines · 2026Review
- Prenatal Melatonin Modulates Cardiovascular Function and Oxidative Stress in Guinea Pig Neonates Under Normoxic and Hypoxic Gestation.Antioxidants (Basel, Switzerland) · 2026Article
- Small Molecules Targeting Mitochondria: A Mechanistic Approach to Combating Doxorubicin-Induced Cardiotoxicity.Cardiovascular toxicology · 2025Review
- α-Tocotrienol Protects Neurons by Preventing Tau Hyperphosphorylation via Inhibiting Microtubule Affinity-Regulating Kinase Activation.International journal of molecular sciences · 2024Article
- Central Causation of Autism/ASDs via Excessive [CaBrain sciences · 2024Review
- Oxidative Stress in Sepsis: A Focus on Cardiac Pathology.International journal of molecular sciences · 2024Article
- Neuroinflammatory Response and Redox-regulation Activity of Hyperoside in Manganese-induced Neurotoxicity Model of Wistar Rats.Current aging science · 2024Article
- Pulmonary Hypertension and Right Ventricle: A Pathophysiological Insight.Clinical Medicine Insights. Cardiology · 2024Review
- Incidence, Risk Factors and Effective Treatment Strategies for Chylothorax After Pediatric Heart Surgeries: Retrospective Analysis of Large Database in Single Institution.Journal of the Saudi Heart Association · 2023Article
- iNOS contributes to heart failure with preserved ejection fraction through mitochondrial dysfunction and Akt S-nitrosylation.Journal of advanced research · 2023Article
- Low Intensity Electromagnetic Fields Act via Voltage-Gated Calcium Channel (VGCC) Activation to Cause Very Early Onset Alzheimer's Disease: 18 Distinct Types of Evidence.Current Alzheimer research · 2022Article
- miRNAs may play a major role in the control of gene expression in key pathobiological processes in Chagas disease cardiomyopathy.PLoS neglected tropical diseases · 2020Article
- Myeloid-Derived Suppressor Cells in Colorectal Cancer.Frontiers in immunology · 2020Review
- Bradykinin Type 1 Receptor - Inducible Nitric Oxide Synthase: A New Axis Implicated in Diabetic Retinopathy.Frontiers in pharmacology · 2019Article
- A Molecular Neurobiological Approach to Understanding the Aetiology of Chronic Fatigue Syndrome (Myalgic Encephalomyelitis or Systemic Exertion Intolerance Disease) with Treatment Implications.Molecular neurobiology · 2018Review
- Disease Tolerance and Pathogen Resistance Genes May UnderlieFrontiers in immunology · 2018Article
- Integration of miRNA and gene expression profiles suggest a role for miRNAs in the pathobiological processes of acute Trypanosoma cruzi infection.Scientific reports · 2017Article
- Low Nasal NO in Congenital Heart Disease With Systemic Right Ventricle and Postcardiac Transplantation.Journal of the American Heart Association · 2017Observational
- Targeting TRAF3IP2 by Genetic and Interventional Approaches Inhibits Ischemia/Reperfusion-induced Myocardial Injury and Adverse Remodeling.The Journal of biological chemistry · 2017Article
- A large scale Plasmodium vivax- Saimiri boliviensis trophozoite-schizont transition proteome.PloS one · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NO/ONOO-cycle is a primarily local, biochemical vicious cycle mechanism, centered on elevated peroxynitrite and oxidative stress, but also involving 10 additional elements: NF-κB, inflammatory cytokines, iNOS, nitric oxide (NO), superoxide, mitochondrial dysfunction (lowered energy charge, ATP), NMDA activity, intracellular Ca(2+), TRP receptors and tetrahydrobiopterin depletion. All 12 of these elements have causal roles in heart failure (HF) and each is linked through a total of 87 studies to specific correlates of HF. Two apparent causal factors of HF, RhoA and endothelin-1, each act as tissue-limited cycle elements. Nineteen stressors that initiate cases of HF, each act to raise multiple cycle elements, potentially initiating the cycle in this way. Different types of HF, left vs. right ventricular HF, with or without arrhythmia, etc., may differ from one another in the regions of the myocardium most impacted by the cycle. None of the elements of the cycle or the mechanisms linking them are original, but they collectively produce the robust nature of the NO/ONOO-cycle which creates a major challenge for treatment of HF or other proposed NO/ONOO-cycle diseases. Elevated peroxynitrite/NO ratio and consequent oxidative stress are essential to both HF and the NO/ONOO-cycle.
Indexed as
Identifiers
What Socratic 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 Socratic graph.