ArticleCardiovascular therapeutics2026
Mechanistic Investigation of Salidroside Modulates Iron Overload to Mitigate Radiation-Induced Heart Disease.
Article in Cardiovascular therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
objectiveRadiation-induced heart disease (RIHD) severely compromises the long-term survival of cancer patients. Although ferroptosis has been implicated as a key contributor to RIHD pathogenesis, the underlying regulatory mechanisms remain incompletely defined. Prompted by clinical observations of elevated serum iron concentrations following thoracic radiotherapy, this study investigated iron-metabolic alterations during RIHD progression and evaluated the cardioprotective efficacy of salidroside in mitigating ferroptosis through restoration of iron homeostasis.
methodsIn a retrospective cohort of 98 patients undergoing thoracic radiotherapy, clinical data were collected, and serum iron concentrations were measured before and after treatment. To elucidate the underlying mechanisms, an RIHD mouse model was established using single-dose precordial irradiation at 20 Gy, followed by salidroside administration. Cardiac function, mitochondrial integrity, and ferroptosis-related markers were systematically assessed. Mechanistic targets were identified using bulk and single-cell RNA sequencing and subsequently validated by molecular docking and Western blotting.
resultsClinical analysis revealed significantly elevated serum iron concentrations after radiotherapy (p < 0.05). Consistent with this clinical phenotype, irradiated mice exhibited cardiac dysfunction, mitochondrial damage, and disrupted iron metabolism. Multiomics analyses identified the transferrin receptor 1 (TFRC) as a potentially critical regulator of these pathological processes. Salidroside treatment significantly ameliorated cardiac injury and attenuated ferroptosis-related alterations. KEGG pathway analysis further demonstrated enrichment of TFRC in the HIF-1 signaling pathway, and salidroside reduced HIF-1α expression, suggesting attenuation of irradiation-associated hypoxic-stress signaling.
conclusionsThoracic radiotherapy may promote RIHD pathogenesis by inducing disrupted iron homeostasis, thereby contributing to cardiomyocyte ferroptosis and mitochondrial injury. Salidroside effectively ameliorates myocardial damage by attenuating iron overload and ferroptosis. Collectively, these findings highlight the translational potential of salidroside as a promising adjunctive cardioprotective agent for patients undergoing thoracic radiotherapy.
Indexed as
Identifiers
42720006What 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.