SVF
Level C· Early Human ResearchProspective Study

Omega-3 PUFAs reduce inflammation by targeting NRF2 and NF-κB activity in an ex vivo model of cardiac mature adipocytes and adipose derived stem cells from atherosclerotic patients.

Quarta S., Santarpino G., Calabriso N., Carluccio MA., Siracusa L., Strano T.

Prospective Study on Cardiovascular Disease, Chronic Inflammation, published in Food Funct (2026) — summary generated from the PubMed abstract.

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Prospective Study
Journal
Food Funct (2026)
Country
England
Reported sample size
—
PMID
41540940
DOI
10.1039/d5fo03219a

Abstract (original English)

Under proatherogenic conditions, epicardial (EAT) and pericardial adipose tissue (PAT) acquire inflammatory/pro-atherogenic phenotypes that contribute to coronary atherosclerosis. Recent data have highlighted a significant inverse relationship between levels of n-3 polyunsaturated fatty acids (PUFAs) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in adipose tissue and risk of myocardial infarction. Our study aimed at investigating whether DHA/EPA supplementation of cardiac fat adipocytes attenuates cardiac adipose tissue inflammation. To this aim mature adipocytes and adipose stem cells were isolated from PAT samples collected from coronary artery disease (CAD) patients undergoing coronary artery bypass grafting, exposed to DHA/EPA ex vivo , and evaluated for pro-inflammatory gene expression and activity. PAT adipocytes and stem cell exposure to DHA led to a significant increase in the membrane ratio of omega-3 to omega-6 PUFAs and decreased mRNA expression levels of monocyte chemoattractant protein (MCP)-1, interleukin(IL)-6, matrix metalloproteinase(MMP)-9 and CXC motif chemokine ligand (CXCL)10 ( p < 0.05). This downregulation was accompanied by increased expression of uncoupling proteins (UCP)1 and 2 and heme-oxygenase (HO)-1 and of the anti-inflammatory and pro-resolving lipid mediator resolvin D1. Mechanistically, this protective modulation appears to be drive

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.

Evidence level

Early human evidence such as case series or small samples, often without a control group.

How we grade evidence
HumansNF-E2-Related Factor 2NF-kappa BAdipocytesFatty Acids, Omega-3Stem CellsInflammationMaleFemaleMiddle Aged
HipSystemic / IVCardiovascular DiseaseChronic Inflammation
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