Key result
Novel biomarkers and imaging refine heart failure risk stratification beyond standard natriuretic peptides.
Why the study?
Oxidative stress contributes to HF progression beyond hemodynamic overload, motivating an evaluation of the relationship between redox imbalance, Galectin-3, fibrosis, and imaging findings.
Integrating redox biomarkers, Galectin-3, and imaging phenotypes may improve heart failure risk stratification and phenotyping beyond standard hemodynamic assessment with natriuretic peptides.
May complement natriuretic peptides for HF phenotyping; leaves open prospective validation of integrated redox-Galectin-3-imaging approaches.
Oxidative stress contributes to heart failure (HF) progression by mechanisms that go beyond hemodynamic overload, including mitochondrial dysfunction, endothelial injury, inflammation, and fibrotic remodeling. This review evaluates the relationship between redox imbalance, Galectin-3 (Gal-3), fibrosis, and imaging findings in HF. Reactive oxygen species (ROS) generated by mitochondria, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, and xanthine oxidase may disturb calcium handling, impair mitochondrial function, activate fibroblasts, and promote ferroptosis. Biomarkers of oxidative injury and antioxidant reserve, including malondialdehyde (MDA), 8-hydroxy-2′-deoxyguanosine (8-OHdG), and circulating thiols, provide information complementary to natriuretic peptides. Experimental evidence supports a context-dependent role of Gal-3 in fibro-inflammatory remodeling, whereas circulating Gal-3 should be regarded as a complementary biomarker rather than as a direct measure of myocardial fibrosis. Echocardiography assesses functional remodeling through diastolic indices, myocardial deformation, and right ventricular–pulmonary arterial (RV–PA) coupling, while cardiac magnetic resonance characterizes focal scar and diffuse interstitial remodeling using late gadolinium enhancement, native T1 mapping, and extracellular volume fraction. Therapeutic strategies are increasingly shifting from nonspecific antioxidant supplementation toward targeting ROS sources and downstream pathways, with SGLT2 inhibitors emerging as clinically relevant agents with indirect redox-modulating effects. Integrated redox, fibro-inflammatory, hemodynamic, and imaging phenotyping may refine risk stratification, although prospective validation is required before routine implementation.
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Ardelean et al. (2026) conducted a review in Heart failure. Multimarker assessment (redox biomarkers, Galectin-3, and imaging) was evaluated. Integrating redox biomarkers, Galectin-3, and imaging phenotypes provides complementary information to natriuretic peptides, refining heart failure phenotyping and risk stratification.
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