Dr. Ramaroson Andriantsitohaina from the Université de Montpellier, France will present a lecture entitled “Extracellular Vesicles in Cardiometabolic Medicine: Biomarkers, Mechanisms, and Therapies” at Targeting Extracellular Vesicles 2026.

Extracellular vesicles (EVs) are emerging as actionable biological messages at the interface of inflammation, vascular injury, metabolic dysfunction and organ crosstalk. Beyond passive biomarkers, EVs carry disease-specific cargo that can identify risk, reveal causal mechanisms and define therapeutic targets.

In metabolic syndrome, circulating EVs carrying NLRP3 inflammasome components identify inflammatory cardiometabolic risk and promote endothelial permeability, monocyte recruitment, vascular remodeling and plaque inflammation, positioning EV-NLRP3 as both biomarker and therapeutic target (Vidal-Gómez et al., Cell Commun and Signal, 2025). In insulin resistance, human
EVs transfer metabolic dysfunction to mice: large EVs carry active PTP1B, whereas small EVs carry PP2A; inhibition of these phosphatases restores IRS1/Akt signalling, defining EV-carried enzymes as druggable mediators of metabolic disease (Ali et al., Diabetologia, 2025).

In MASLD/MASH, faeces-derived EVs and circulating EVs connect gut dysbiosis to liver injury. NASHfEVs disrupt intestinal barrier integrity through nmMLCK, activate endothelial inflammation via LPS/TLR4, and stimulate hepatic inflammatory and fibrotic pathways, supporting fEVs as biomarkers, bioeffectors and therapeutic targets in the gut–liver axis (Fizanne et al., J Extracell Vesicles, 2023).

Engineered small EVs now open a therapeutic frontier. Systemic SF1-AMPKα1-DN sEVs target VMH–SF1 hypothalamic neurons, induce feeding-independent weight loss, activate brown adipose tissue thermogenesis and promote white adipose tissue browning in diet-induced and genetic obesity (Milbank et al., Nature Metabolism, 2021; Metabolism, 2023). New breakthrough data further suggest that SF1-NLRP3-DN-EVs may rebalance autonomic control and reduce obesity-associated atrial fibrillation, inflammation and fibrosis.

Recent outcome trials, including SELECT, STEP-HFpEF and SURMOUNT-OSA, confirm that targeting obesity-driven cardiometabolic disease improves cardiovascular, heart-failure and sleep-apnea outcomes (Lincoff et al., NEJM, 2023; Kosiborod et al., NEJM, 2023; Malhotra et al., NEJM, 2024).

Together, these data support a new paradigm: EVs reveal biomarkers, define targets and may become precision therapies to reprogram cardiometabolic disease