ArticleScientific reports2026
8-OHdG and NT-proBNP as complementary biomarkers in the postmortem diagnosis of acute ischemic heart disease.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Evaluating the impact of blue-filtering intraocular lenses on macular oxidative stress: A comparative analysis of 8-hydroxy-2'-deoxyguanosine levels in the retinal tissue of donor eyes.Indian journal of ophthalmology · 2026Article
- Heat Stress in the Liver of Chicken: Insights from Keap1-Nrf2 Pathway Mediated Ferroptosis and Cuproptosis via the HO-1/FDX1/Gpx4 Axis.Veterinary sciences · 2026Article
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9 authors.
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Abstract
Acute ischemic heart disease (AIHD) is a major cause of sudden cardiac death, yet postmortem diagnosis is difficult, particularly in early-phase ischemic injury or decomposed bodies. We investigated the diagnostic value of two molecular biomarkers—8-hydroxy-2′-deoxyguanosine (8-OHdG), indicating oxidative DNA damage, and N-terminal pro-brain natriuretic peptide (NT-proBNP), reflecting cardiac wall stress—in 67 human forensic autopsy cases (33 AIHD, 34 non-AIHD). Immunohistochemistry revealed significantly greater and more diffuse nuclear 8-OHdG expression in AIHD cardiomyocytes compared with controls. Postmortem blood NT-proBNP levels were also significantly higher in AIHD cases (2389.1 ± 499.6 pg/mL) than in non-AIHD cases (896.1 ± 190.1 pg/mL). No significant correlations were found between 8-OHdG expression and NT-proBNP levels, contraction band necrosis, postmortem interval, age, or sex, suggesting that these markers reflect distinct pathological processes—oxidative injury and hemodynamic stress. Both markers demonstrated postmortem stability, and their combined evaluation improved diagnostic confidence in cases with inconclusive histology. This dual-biomarker approach may enhance the accuracy of AIHD diagnosis in forensic practice and provide complementary insights into the molecular mechanisms underlying sudden cardiac death.
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