bims-evecad 2026-03-22 papers

Issue of 2026–03–22
two papers selected by
Cliff Dominy

J Extracell Vesicles. 2026 Mar;15(3): e70254

The Fatty Acid Transporter CD36 Mediates Uptake, Biodistribution, and Cardioprotection by Small Extracellular Vesicles From HEK293 Cells.

Elias Sulaiman, Derek M Yellon, Sean M Davidson.

Extracellular vesicles (EVs) are nanoscale carriers of bioactive molecules that mediate intercellular communication. Small EVs (sEVs) have shown cardioprotective effects in models of myocardial infarction (MI), but their uptake and biodistribution remain incompletely understood. Here, we investigated NanoLuc-labelled HEK293-derived sEVs, assessing their uptake in cardiac cells, in vivo biodistribution, and effect on infarct size following cardiac ischaemia and reperfusion (IR) injury. We hypothesised that the scavenger receptor CD36, a lipid-binding receptor expressed in both cardiomyocytes and endothelial cells, may mediate sEV uptake. sEVs were purified by size-exclusion chromatography and tangential flow filtration. In vitro, cardiac endothelial cells internalised sEVs more efficiently than cardiomyocytes. In healthy mice, sEVs accumulated mainly in the lungs, liver, and spleen. However, when administered post-IR, sEVs significantly reduced infarct size (from 58% ± 8% to 36% ± 3%, p < 0.05, n = 5). Inhibition of CD36 with sulfosuccinimidyl oleate impaired sEV uptake and abolished cardioprotection. These findings suggest HEK293-sEVs may have therapeutic potential in MI and identify CD36 as a key mediator of their uptake and function.

Keywords: CD36; biodistribution; cardioprotection; extracellular vesicles; ischaemia; mice; nanoluciferase; reperfusion

DOI: https://doi.org/10.1002/jev2.70254

iScience. 2026 Apr 17. 29(4): 115151

Adipose extracellular vesicles carrying miR-210-3p drive macrophage inflammation and nicotine-induced atherosclerosis.

Yanchao Li, Mengyue Yang, Hongyu Li, Yiyi Lei, Meng Zhang, Ziyu Yang, Xingtao Huang, Yufei Sun, Qi Liu, Xuedong Wang, Jingbo Hou.

Visceral adipose tissue (VAT)-derived extracellular vesicles (EVs) have emerged as key mediators of inter-organ communication, yet their role in nicotine-induced atherosclerosis remains poorly defined. Here, we demonstrate that nicotine markedly enhances secretion of VAT-EVs and that these EVs are preferentially internalized by macrophages within atherosclerotic plaques, thereby accelerating lesion progression. Functionally, nicotine-induced VAT-EVs promote macrophage inflammation, oxidative stress, and foam cell formation. High-throughput profiling identified miR-210-3p as a dominant pro-atherogenic cargo within VAT-EVs, and its inhibition significantly attenuated nicotine-induced atherosclerosis in vivo. Mechanistically, miR-210-3p directly targets Krüppel-like factor 7 (KLF7), amplifying macrophage inflammatory responses and promoting plaque progression. Collectively, these findings uncover a previously unrecognized role of adipose-derived EVs in smoking-related vascular injury and highlight EV-derived miR-210-3p as a promising therapeutic target in nicotine-associated atherosclerosis.

Keywords: cardiovascular medicine; molecular biology experimental approach; molecular medicine

DOI: https://doi.org/10.1016/j.isci.2026.115151