Hormonal
Obesity increases atherosclerosis susceptibility via an endocrine-like mechanism where adipose-derived miR-30e-5p travels to vascular endothelial cells, downregulates SLC7A11, and impairs mitochondrial function.
This research highlights that obesity is not just a passive storage of fat but an active endocrine organ that sends damaging signals to blood vessels. Managing body weight is crucial to stop adipose tissue from releasing miR-30e-5p, which directly harms the lining of your arteries and promotes plaque buildup, independent of cholesterol levels.
Our multi-omics approaches demonstrates that the adipose-derived miR-30e-5p downregulated SLC7A11 mRNA in ECs via tissue crosstalk. The resulting EC dysfunction led to obesity-related atherosclerosis in mice.
Why this rating
The study uses robust multi-omics, human patient data, and multiple mouse models, but it is a preprint and relies on animal models for causality.
Source
Obesity Increases Atherosclerosis Susceptibility via Inter-tissue miR-30e-SLC7A11 Axis
Chen Wang et al. · bioRxiv (Cold Spring Harbor Laboratory) · 2025
DOI 10.1101/2025.03.06.641950
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