Circulating Extracellular Vesicles in the Pathogenesis of Heart Failure in Patients With Chronic Kidney Disease
Authors' conclusion
Collectively, our human subject and mouse studies show that circulating CKD-EVs, carrying distinct renal-derived miRNAs, mediate the molecular crosstalk that contributes to the pathogenesis of heart failure in CKD.
Study context
- Population
- Patients with chronic kidney disease (CKD); adenine diet-induced CKD mice
- Comparison
- CKD-EVs vs control extracellular vesicles (EVs)
Methodological detailscross-sectional, human and mouse studies
- Cross-sectional
- Human and mouse studies
Main finding
As reported in the abstract
- Plasma EVs from CKD patients, but not healthy controls, cardiotoxic: induced apoptosis in vitro and in vivo and impaired contractility of adult rat primary cardiomyocytes
- EVs from plasma and kidneys of CKD mice cardiotoxic
- Pharmacological depletion of circulating EVs in CKD mice significantly recovered cardiac function and ameliorated HF
- Human and mouse CKD-EVs enriched in distinct microRNA (miRNAs) vs control EVs
- CKD-EV-miRNA mimics cardiotoxic: impaired contractility and downregulated contractile gene expression in human iPSC-derived cardiomyocytes
- Corresponding primary miRNAs significantly higher in CKD kidney tissue (CD45-veCD31-ve renal cells), not in CKD hearts, livers or PBMCs: renal origin
- CKD-EV-miRNA levels correlated with established markers of cardiac injury
Original publication
Circulating Extracellular Vesicles in the Pathogenesis of Heart Failure in Patients With Chronic Kidney Disease. Circulation. Published 3 November 2025. doi:10.
Summarised from the published abstract; every number is checked against it