ReviewFrontiers in pharmacology2025
Research progress in the prevention and treatment of radiation-induced heart disease.
Review in Frontiers in pharmacology, 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
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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.
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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.
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Who cites it
3 citing papers in PubMed.
- Nutritional Prevention of Oxidative Stress-Induced Cardiotoxicity in Pediatric Cardio-Oncology: Molecular Mechanisms and Translational Perspectives-A Narrative Review.International journal of molecular sciences · 2026Review
- Endothelial dysfunction: A central mechanism linking autosomal dominant polycystic kidney disease and intracranial aneurysms (Review).International journal of molecular medicine · 2026Review
- Metabolic reprogramming in radiation-induced heart disease: the emerging role of PET imaging.Frontiers in cardiovascular medicine · 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiotherapy (RT) is a cornerstone treatment for thoracic malignancies, but is associated with an increased risk of radiation-induced heart disease (RIHD), a major cause of long-term morbidity and mortality in cancer survivors. Ionizing radiation directly damages cellular components (proteins, lipids, and DNA), disrupts the mitochondrial electron transport chain, and activates enzymes such as NADPH oxidases, this leads to excessive production and accumulation of reactive oxygen species (ROS). Oxidative stress triggers the pro-inflammatory NF-κB pathway, pro-oxidative MAPK branch of IGF-1 signaling, and the pro-fibrotic TGF-β1 pathway. These cascades promote chronic inflammation, endothelial dysfunction, and microvascular damage, leading to myocardial fibrosis and dysfunction. Antioxidant and anti-inflammatory therapies represent a promising approach for the clinical management of RIHD. Preclinical evidence has suggested that statins, angiotensin-converting enzyme inhibitors (ACEIs), and natural antioxidants such as sodium Tanshinone IIA sulfonate mitigate RIHD by scavenging ROS, reducing inflammation, and inhibiting fibrosis. However, further clinical validation of these drugs is required for RIHD. This review highlights the current research status of the known pathophysiological mechanisms of RIHD, and the various treatment strategies used for its prevention and treatment.
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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.