ReviewCells2026
Multicellular Communication Networks in Myocardial Ischemia-Reperfusion Injury: Spatial and Temporal Organization of Injury and Repair.
Review in Cells, 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
2 authors.
Funding
Abstract
Myocardial ischemia-reperfusion injury (MIRI) complicates recovery after acute myocardial infarction despite timely restoration of coronary blood flow. Beyond cardiomyocyte-intrinsic oxidative stress, calcium dysregulation, mitochondrial injury, and regulated cell death, reperfusion simultaneously reorganizes communication among multiple cardiac and extracardiac cell populations. Single-cell and spatial multiomic studies further reveal marked spatial and temporal heterogeneity across the injured heart, although the causal intercellular mechanisms underlying many associations remain incompletely defined. In this Review, we examine MIRI through a multicellular communication framework and discuss interactions among cardiomyocytes, immune cells, endothelial cells, platelets, fibroblasts, vascular mural cells, and extracardiac tissues across the infarct core, border zone, coronary microvascular unit, and remote myocardium. Communication occurs through soluble danger and inflammatory signals, selected metabolites, extracellular vesicles, extracellular matrix and mechanical cues, and direct contact or junctional mechanisms. We distinguish experimentally supported intercellular pathways from spatial associations, parallel responses, and indirect regulatory mechanisms. A spatiotemporally resolved view of these networks may help identify interactions that amplify injury, impair microvascular reperfusion, or participate in resolution and repair, while guiding selective interventions that limit pathological signaling without compromising tissue recovery.
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Registered trials
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