ReviewRedox biology2026
Mitochondrial heterogeneity across cardiac cell types in heart failure with preserved ejection fraction.
Review in Redox biology, 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
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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.
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.
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Authors and funding
4 authors.
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Abstract
Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous and increasingly prevalent syndrome for which effective disease-modifying therapies remain limited, in part because its multicellular pathophysiology remains incompletely understood. Mitochondrial dysfunction has emerged as an important contributor to HFpEF, yet most studies have examined mitochondrial abnormalities within individual cell types rather than as part of an integrated cardiac microenvironment. This review discusses evidence that cell-type-specific mitochondrial alterations in cardiomyocytes, fibroblasts, and endothelial cells may interact through redox, metabolic, and paracrine signaling to promote diastolic dysfunction, myocardial stiffening, and impaired energetic reserve. In cardiomyocytes, disrupted mitochondrial calcium (
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