ReviewHeliyon2024
Ferroptosis in diabetic cardiomyopathy: Advances in cardiac fibroblast-cardiomyocyte interactions.
Review in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 9 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
9 citing papers in PubMed.
- Ion channels and GPCRs as pharmacological regulators of ferroptosis and pyroptosis in metabolic diseases.Diabetology & metabolic syndrome · 2026Review
- The Regulatory Landscape of Ferroptosis and Iron Homeostasis: Pathophysiological Mechanisms and Therapeutic Horizons in Cardiovascular Disease.Drug design, development and therapy · 2026Review
- Oxidative stress and ferroptosis in diabetic cardiomyopathy: mechanistic interplay and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2025Review
- Ferroptosis in the pathogenesis of diabetic cardiomyopathy: mechanisms and therapeutic potential.Cardiovascular diabetology · 2025Review
- Bone marrow mesenchymal stem cells-derived exosomes protect against β-cell destruction models and kidney injury by suppressing ferroptosis.Scientific reports · 2025Article
- DNA-PKcs-Driven YAP1 Phosphorylation and Nuclear Translocation: a Key Regulator of Ferroptosis in Hyperglycemia-Induced Cardiac Dysfunction in Type 1 Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Integrative single-cell and multi-omics analyses reveal ferroptosis-associated gene expression and immune microenvironment heterogeneity in gastric cancer.Discover oncology · 2025Article
- Identification of lipid metabolism-related genes in dapagliflozin treated rats with diabetic cardiomyopathy by bioinformatics.Frontiers in endocrinology · 2025Article
- New insights into FGF21 alleviates diabetic cardiomyopathy by suppressing ferroptosis: a commentary.Cardiovascular diabetology · 2024Article
Corrections and comments
- Expression of concern
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic cardiomyopathy (DCM) is a common complication of diabetes, and its pathogenesis remains elusive. Ferroptosis, a process dependent on iron-mediated cell death, plays a crucial role in DCM via disrupted iron metabolism, lipid peroxidation, and weakened antioxidant defenses. Hyperglycemia, oxidative stress, and inflammation may exacerbate ferroptosis in diabetes. This review emphasizes the interaction between cardiac fibroblasts and cardiomyocytes in DCM, influencing ferroptosis occurrence. By exploring ferroptosis modulation for potential therapeutic targets, this article offers a fresh perspective on DCM treatment. The study systematically covers the interplay, mechanisms, and targeted drugs linked to ferroptosis in DCM development.
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.