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Extracellular Vesicles Modulation by an Adiponectin Receptor Agonist Provides Cardioprotection for Myocardial
Jialing Tang1, Wing Yan Chung1, Serena M Pulente2
1Department of Biology, York University, Toronto, Ontario, Canada.
Advanced Healthcare Materials
|April 14, 2026
Summary
Adiponectin receptor agonist ALY688 enhances extracellular vesicles (EVs) to protect the heart after myocardial infarction (MI). This therapy improves cardiac function and reduces injury by modulating EV cargo and function.
Area of Science:
- Cardiovascular Biology
- Regenerative Medicine
- Cellular Signaling
Background:
- Ischemic heart disease is a major global health burden requiring novel therapeutic strategies.
- Extracellular vesicles (EVs) play a critical role in intercellular communication within the heart.
- Adiponectin is known for its cardioprotective effects, but its interaction with EVs in cardiac injury is not well understood.
Purpose of the Study:
- To investigate if ALY688, an adiponectin receptor agonist, can modify EV biogenesis and cargo for cardioprotection in a mouse model of myocardial infarction (MI).
- To elucidate the mechanisms by which ALY688-modified EVs exert their protective effects.
Main Methods:
- Administration of ALY688 to mice subjected to myocardial infarction.
- Isolation and characterization of plasma EVs.
- Proteomic analysis of EVs.
- In vitro studies using iPSC-derived cardiomyocytes and H9c2 cells.
- In vivo assessment of therapeutic efficacy and cardiac function.
Main Results:
- ALY688 treatment attenuated cardiac dysfunction, reduced infarct size, and decreased fibrosis in mice with MI.
- ALY688 restored circulating EV numbers post-MI and increased their loading with bioactive adiponectin.
- Proteomic analysis showed EVs from ALY688-treated mice were enriched in metabolism-related proteins.
- EVs from ALY688-treated mice (EVALY) protected cardiomyocytes from hypoxia-induced apoptosis, reduced ROS, restored mitochondrial function, and enhanced autophagy.
- Systemic administration of EVALY reduced cardiac injury markers, apoptosis, and improved mitochondrial dynamics in vivo.
Conclusions:
- ALY688 enhances EV-mediated cardioprotection by improving adiponectin delivery, reducing oxidative stress, restoring autophagy, and recovering mitochondrial function.
- These findings suggest that modulating endogenous EVs via adiponectin receptor agonism is a promising therapeutic strategy for acute cardiovascular injury.
