ReviewAntioxidants (Basel, Switzerland)2025
Roles of Autophagy and Oxidative Stress in Cardiovascular Disease.
Review in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Diet-Induced Ceramide Remodeling as a Mechanistic Link to Cardiac Metabolic Dysfunction.Nutrients · 2026Review
- Review
- Review
- Targeting the AMPK Pathway with Natural Products for Heart Failure: A Systematic Review of Preclinical Evidence.Biomedicines · 2026Review
- Hypoxia, ROS, and HIF Signaling in I/R Injury: Implications and Future Prospects.Antioxidants (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Autophagy and oxidative stress influence cardiovascular pathology. Autophagy mediates lysosome-dependent clearance of damaged proteins and organelles and maintains mitochondrial quality control, proteostasis, and metabolic flexibility. Reactive oxygen species (ROS) originate from mitochondrial respiration and enzymatic reactions during stress. At physiological levels, ROS function as redox signals that activate degradation and recycling, whereas excess oxidants damage lipids, proteins, and nucleic acids and promote cell loss. This review integrates evidence across cardiovascular disease, including atherosclerosis, ischemia reperfusion injury, pressure overload remodeling, heart failure, diabetic cardiomyopathy, arrhythmia, aging, and inflammation.
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.