ReviewMolecular biology reports2025
Beyond conventional therapy: NOX4 as a promising target in cardiomyopathy.
Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Cardioprotective Role of CalhexCell biochemistry and biophysics · 2026Review
- Predictors of right ventricular dysfunction and its clinical value after reperfusion of acute right coronary artery occlusion: a single-center retrospective analysis.American journal of translational research · 2026Article
- A new KLF13 loss-of-function mutation responsible for sporadic dilated cardiomyopathy.Molecular biology reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiomyopathy refers to disorders marked by structural and functional irregularities in the heart muscle, occurring independently of other conditions that might explain these abnormalities. The most common types are dilated and hypertrophic cardiomyopathies, while Takotsubo, restrictive, left ventricular non-compaction, and arrhythmogenic right ventricular cardiomyopathies are rarer. These conditions cause ventricular hypertrophy, fibrosis, myocardial dysfunction, and chamber dilation due to responses to stressors such as pressure overload, myocardial infarction, inflammation, diabetes, and cardiotoxic drugs. Oxidative stress, marked by an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, plays a key role in the cardiac pathophysiology of various cardiomyopathy subtypes. In the heart, ROS are mainly generated by NADPH oxidase (NOX) under normal and pathological conditions. NADPH oxidase 4 (NOX4) is a major source of ROS within cardiomyocyte mitochondria. Research shows that ROS produced by NOX4 contribute to pathological cardiac remodeling, myocardial inflammation, fibrosis, apoptosis, genetic mutations, and hypertrophy. NOX4 inhibition or deletion alleviates these harmful effects. This review explores NOX4-driven ROS production across cardiomyopathy subtypes and its implications. Understanding the roles of NOX4 in cardiac health will help develop innovative therapeutic strategies for preventing and managing cardiomyopathy. This review aims to provide a synthesis of current knowledge regarding NOX4's function and regulatory mechanisms in cardiomyopathy.
Indexed as
Identifiers
40643777What 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.