ArticleMolecular medicine reports2021
Radiation‑induced dysfunction of energy metabolism in the heart results in the fibrosis of cardiac tissues.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 38 citations in OpenAlex.
- Sex differences in a mouse model of radiation-induced cardiotoxicity.Research square · 2026Article
- ATOX1 alleviates radiation-induced cardiac injury by modulating AMPK/NRF2 to inhibit myocardial oxidative stress and mitochondrial dysfunction.Journal of cell communication and signaling · 2026Article
- Cardioprotective Effect and Mechanism of Panaxadiol Saponin Component in Radiation-Induced Heart Disease in Mice.Chinese journal of integrative medicine · 2026Article
- Chemo-/radiotherapy-induced cardiomyopathy: roles of mitochondria and endoplasmic reticulum.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2026Review
- Mitochondrial damage and post-translational modifications in radiation-induced heart disease: mechanisms and emerging therapeutic targets.Frontiers in pediatrics · 2026Review
- Multiple radiations and its effect on biological system - a review onAnnals of medicine · 2025Review
- Radiation meets inflammation: NLRP3 inflammasome at the core of radiation-induced cardiac injury.Journal of translational medicine · 2025Review
- Metabolomic effects of total flavone of Abelmoschus manihot (L.) medik. on patients with radiation-induced heart disease.Scientific reports · 2025Article
- Exploring mechanisms of radiation-induced myocardial fibrosis using HMGB1 neutralizing antibody.Journal of molecular histology · 2025Article
- The impact of citicoline on brain mitochondrial dysfunction induced in rats after head irradiation.Scientific reports · 2025Article
- ALKBH5 exacerbates early cardiac damage after radiotherapy for breast cancer via m6A demethylation of TLR4.Open life sciences · 2025Article
- Advances in mitochondrial dysfunction in radiation tissue injury.Frontiers in physiology · 2025Review
- Article
- Sirtuin 2 Exerts Regulatory Functions on Radiation-Induced Myocardial Fibrosis in Mice by Mediating H3K27 Acetylation of Galectin-3 Promoter.Acta Cardiologica Sinica · 2024Article
- Organs in orbit: how tissue chip technology benefits from microgravity, a perspective.Frontiers in lab on a chip technologies · 2024Article
- Delayed effects of radiation in adipose tissue reflect progenitor damage and not cellular senescence.GeroScience · 2023Article
- Article
- Acetylation of Atp5f1c Mediates Cardiomyocyte Senescence via Metabolic Dysfunction in Radiation-Induced Heart Damage.Oxidative medicine and cellular longevity · 2022Article
- Case report: Stereotactic body radiation therapy with 12 Gy for silencing refractory ventricular tachycardia.Frontiers in cardiovascular medicine · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thoracic radiotherapy increases the risk of radiation‑induced heart damage (RIHD); however, the molecular mechanisms underlying these changes are not fully understood. The aim of the present study was to investigate the effects of radiation on the mouse heart using high‑throughput proteomics. Male C57BL/6J mice were used to establish a model of RIHD by exposing the entire heart to 16 Gy high‑energy X‑rays, and cardiac injuries were verified using a cardiac echocardiogram, as well as by measuring serum brain natriuretic peptide levels and conducting H&E and Masson staining 5 months after irradiation. Proteomics experiments were performed using the heart apex of 5‑month irradiated mice and control mice that underwent sham‑irradiation. The most significantly differentially expressed proteins were enriched in 'cardiac fibrosis' and 'energy metabolism'. Next, the cardiac fibrosis and changes to energy metabolism were confirmed using immunohistochemistry staining and western blotting. Extracellular matrix proteins, such as collagen type 1 α 1 chain, collagen type III α 1 chain, vimentin and CCCTC‑binding factor, along with metabolism‑related proteins, such as fatty acid synthase and solute carrier family 25 member 1, exhibited upregulated expression following exposure to ionizing radiation. Additionally, the myocardial mitochondria inner membranes were injured, along with a decrease in ATP levels and the accumulation of lactic acid in the irradiated heart tissues. These results suggest that the high doses of ionizing radiation used lead to structural remodeling, functional injury and fibrotic alterations in the mouse heart. Radiation‑induced mitochondrial damage and metabolic alterations of the cardiac tissue may thus be a pathogenic mechanism of RIHD.
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