ArticleAdvanced healthcare materials2026
Extracellular Vesicles Modulation by an Adiponectin Receptor Agonist Provides Cardioprotection for Myocardial Ischemic Injury.
Article in Advanced healthcare materials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
- ALY688 Protects Against Myocardial Ischemia-Reperfusion Injury via Direct Effects and Rab8a-Dependent Extracellular Vesicles.Journal of extracellular vesicles · 2026Article
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Authors and funding
14 authors.
Funding
Abstract
Ischemic heart disease is a leading cause of global morbidity and mortality, with more effective clinical therapies needed to mitigate cardiac ischemic injury. Extracellular vesicles (EVs) mediate intercellular communication in cardiac pathophysiology. Adiponectin mediates cardioprotective effects yet its relationship with EVs biology remains unexplored. We investigated whether ALY688, an adiponectin receptor agonist, modulates EV biogenesis and cargo to confer cardioprotection in a mouse model of myocardial infarction (MI). ALY688 (15 mg/kg daily for 28 days) significantly attenuated MI-induced cardiac dysfunction, reduced infarct size, and decreased fibrotic scar in both lean mice on standard chow and obese mice fed a high-fat diet. Plasma EVs were isolated and while MI reduced circulating EV numbers, ALY688 restored EV production and enhanced loading with bioactive adiponectin. In addition, proteomic analysis revealed ALY688-shaped EVs were enriched in metabolism regulated proteins. The direct functional effects and mechanisms of EV action were examined in iPSC-derived cardiomyocytes and H9c2 cells. EV from ALY688 treated mice (EV
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