ReviewInternational journal of molecular sciences2025
Implications of Oxidative Stress in the Pathophysiological Pathways of Heart Failure.
Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed.
- From Oxidative Stress to Fibrotic Remodeling: Integrating Redox Biology, Galectin-3, and Imaging Phenotypes in Heart Failure.Antioxidants (Basel, Switzerland) · 2026Review
- Micro- and Nanoplastics as Potential Drivers of Dilated Cardiomyopathy.Life (Basel, Switzerland) · 2026Review
- Silent Inflammation: A Critical Narrative Review of the Relationship Between Periodontal Disease and Psychosis-The Role of Oxidative Stress and Iatrogenic Comorbidities.Antioxidants (Basel, Switzerland) · 2026Review
- Septic Cardiac Remodeling: A New Concept in Cardiac Dysfunction Induced by Experimental Sepsis.Antioxidants (Basel, Switzerland) · 2026Article
- The Influence of Basic Therapy and New Drugs on NO-Dependent Mechanisms of Cardiac Destruction in Chronic Heart Failure.Biomedicines · 2026Review
- S-nitrosoglutathione preserves vasodilation and attenuates myocardial ischemia-reperfusion injury.Scientific reports · 2026Article
- Gut Microbiota-Derived Trimethylamine N-Oxide and NT-proBNP in Heart Failure: A Critical Review of Diagnostic and Prognostic Value.Biomedicines · 2026Review
- Advances in Diagnosis and Treatment of Acute and Chronic Heart Failure: A Comprehensive Review.Journal of clinical medicine · 2026Review
- Chronic β-Blockade and Systemic Homeostasis: Molecular Integration of Cardiorenal and Immune Pathways, a Narrative Review.Biomolecules · 2025Review
- Oxidative Stress and Postoperative Outcomes: An Umbrella Review of Systematic Reviews and Meta-Analyses.Antioxidants (Basel, Switzerland) · 2025Review
- Epigallocatechin Gallate as a Molecular Therapeutic in Heart Failure and Cardio-Oncology: Mechanistic Pathways and Translational Perspectives.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure (HF) is a major socioeconomic problem worldwide, associated with high morbidity and mortality due to several underlying diseases. HF is driven by several closely linked mechanisms whose effects are mutually reinforcing. Some of the signalling pathways involved in the progression of HF may initially be compensatory, such as the renin-angiotensin-aldosterone system (RAAS), whose hyperactivation plays a central role in the progression of HF by promoting fluid retention, inflammation, oxidative stress (OS), and myocardial dysfunction. Fluid retention is also promoted by the action of neprilysin, which contrasts natriuresis and vasodilation. Among the compensatory and subsequently maladaptive systems, chronic hyperactivation of the sympathetic nervous system (SNS) exacerbates maladaptive remodelling and drives the progression of HF. At the molecular level, mitochondrial dysfunction and inflammatory substances are involved in the development of a state of systemic oxidative stress and inflammation. The aim of the following manuscript was to revise the pathophysiology and role of OS in HF, focusing on the current knowledge of the molecular pathways involved.
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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.