ReviewCureus2026
The Role of Oxidative Stress in Heart Failure: Mechanisms and Therapeutic Targets.
Review in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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.
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Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure is characterised by increased production of reactive oxygen species (ROS), which contribute to apoptotic signalling. Changes in excitation-contraction coupling in heart failure promote increased calcium extrusion and decreased calcium uptake by myocardial mitochondria. Mitochondrial calcium is required to increase the Krebs cycle flux to generate sufficient nicotinamide adenine dinucleotide (NADH) to match the increased energy demand seen in heart failure. Reduced NADH availability can decrease levels of reduced nicotinamide adenine dinucleotide phosphate (NADPH), leading to a loss of NADPH-mediated antioxidant capacity and thereby increasing ROS emission and oxidative damage. Accordingly, a group of therapies that increase mitochondrial calcium, such as sodium glucose-linked transporter 2 inhibitors and ranolazine, have been investigated as potential treatments in heart failure. Proposed mechanisms include reducing calcium extrusion from mitochondria via the Na
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