Table 1.

Summary of the most important studies concerning the role of EAT in the pathogenesis of ACS and cardiac remodeling after MI.

First Author	Year	Study Population/Experimental Model	Main Findings	Reference
Moreno-Santos, I.	2019	Patients with ACS (n = 29), stable CAD (n = 16) or without CAD (n = 29)	Reduced expression of NPR-C, UCP1 and PGC1α in EAT of ACS patients. Decreased activation of p38 MAPK pathway in EAT samples from ACS patients.	[32]
Hao, S.	2023	Male Sprague Dawley rats: MI induction (n = 6) or sham surgery (n = 6); H9C2 cardiomyocytes	After MI, EAT mediates cardiomyocytes’ apoptosis by secretion of CFD, which causes PARP-1 activation.	[33]
Pedicino, D.	2017	Patients with ACS (n = 18), SA (n = 16) or without CAD (n = 13)	Enhanced NLRP3 and pro-IL1β expression in EAT from ACS patients. Many bacterial species were found in EAT samples from ACS and SA patients.	[34]
Parisi, V.	2020	Patients with CCS (n = 54) or recent ACS (n = 33)	Reduced IL-1ra levels in EAT from ACS patients.	[35]
Pedicino, D.	2022	Patients with ACS (n = 32), CCS (n = 34) or MVD (n = 12)	Higher content of CD31, CHI3L1, CRP, ENG, IL-17, IL-33, MMP-9, MPO, NGAL, RBP-4, RETN, in EAT of ACS patients found in proteome profiling. Perturbation of the TRBV21 in EAT were associated with the first NSTEMI.	[36]
Langheim, S.	2010	Patients with ACS (n = 32), stable CAD (n = 34) or without CAD (n = 23); HUVEC	Increased resistin expression in EAT of ACS patients. Supernatant of cultured EAT obtained from ACS patients increased permeability of endothelial cells in vitro. Greater number of CD68+ cells in was found EAT of ACS patients than stable CAD patients and controls.	[37]
Rachwalik, M.	2014	Patients undergoing CABG with history of MI (n = 17) or without previous MI (n = 16)	Previous MI was associated with higher resistin content in EAT.	[38]
Hao, S.	2021	Male Sprague Dawley rats: MI induction (n = 20) or sham surgery (n = 10); H9C2 cardiomyocytes	EAT-CM through miR-134-5p/KAT7/MnSOD/catalase axis and increase in ROS intracellular levels promoted activation of cardiac fibroblasts into myofibroblasts. Knockdown of miR-134-5p limited myocardial fibrosis in vivo.	[39]
Chang, H-X	2017	Sprague Dawley rats (n = 82) which underwent MI (with or without EAT removal) or sham surgery	Increased lipolysis of EAT after MI. EAT removal reduced infarct area, enhanced cardiac function, and decreased inflammation after MI.	[40]

Abbreviations: ACS, acute coronary syndrome; CAD, coronary artery disease; CFD, complement factor D; CHI3L1, chitinase 3-like 1; CRP, C-reactive protein; EAT, epicardial adipose tissue; EAT-CM, conditioned media from epicardial adipose tissue; ENG, endoglin; IL-17, interleukin-17; IL-1ra, interleukin-1 receptor antagonist; IL-33, interleukin-33; KAT7, lysine acetyltransferase 7; MAPK, mitogen-activated protein kinase; MI, myocardial infarction; MMP-9, matrix metallopeptidase 9; MNSOD, manganese superoxide dismutase; MPO, myeloperoxidase; NGAL, neutrophil gelatinase-associated lipocalin (lipocalin 2); NLRP3, NLR family pyrin domain containing 3; NPR-C, natriuretic peptide receptor-C; NSTEMI, non-ST-elevation myocardial infarction; PARP-1, poly(ADP-ribose) polymerase 1; PGC1α, peroxisome proliferator-activated receptor gamma coactivator alpha; pro-IL1β, pro-interleukin-1beta; RBP-4, retinol binding protein 4; RETN, resistin; ROS, reactive oxygen species; SA, stable angina; TRBV21, T cell receptor beta variable 21-1; UCP1, uncoupling protein 1.