Excessive accumulation of epicardial adipose tissue promotes microvascular obstruction formation after myocardial ischemia/reperfusion through modulating macrophages polarization
Authors' conclusion
Our work for the first time demonstrated that excessive accumulation of EAT promoted MVO formation by promoting the polarization state of cardiac macrophages towards an inflammatory phenotype. Furthermore, this study identified a very promising therapeutic strategy, GLP-1/GLP-2 receptor dual agonist, targeting EAT for MVO prevention following myocardial I/R injury.
Study context
- Population
- Patients with STEMI assessed by cardiac magnetic resonance; mouse model of myocardial ischemia/reperfusion injury
- Outcome
- Association of EAT accumulation with MVO formation measured by CMR
Methodological detailsclinical cardiac magnetic resonance (CMR) study, mouse model with epicardial adipose tissue (EAT) depletion, co-culture experiments
- Clinical CMR study
- Mouse model with EAT depletion
- Co-culture experiments
Main finding
As reported in the abstract
MVO formation
- Increase of left atrioventricular EAT mass index independently associated with microvascular obstruction (MVO) formation
- EAT accumulation boosted macrophage transition towards inflammatory phenotype in myocardial I/R injury through secreting inflammatory EVs
Further findings
DPP4
- Increased circulating DPP4 levels and high DPP4 activity seemed to be associated with EAT increase
GLP-1 RA and GLP-1/GLP-2 receptor dual agonist
- Potential therapeutic effects for MVO prevention at least partially ascribed to EAT modulation
Original publication
Excessive accumulation of epicardial adipose tissue promotes microvascular obstruction formation after myocardial ischemia/reperfusion through modulating macrophages polarization. Cardiovasc Diabetol. Published 5 July 2024. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →