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Epicardial adipose tissue (EAT) acts as a cardio-proximal immunometabolic interface influencing atrial fibrillation, heart failure with preserved ejection fraction, and coronary atherogenesis via paracrine signaling. Weight loss only partially reverses obesity-imprinted transcriptional and epigenetic programs, sustaining cardiovascular risk despite metabolic improvement. Resolution pharmacology using specialized pro-resolving mediators and receptors aims to terminate inflammation and reprogram immune–stromal interactions, though clinical translation is limited by pharmacokinetics and biomarker validation gaps. 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Antoniadis 1 and Nikolaos Fragakis 1  \nAcademic Editor: PawelDobrzyn  \nReceived: 8 December 2025  \nRevised: 29 December 2025  \nAccepted: 3 January 2026  \nPublished: 5 January 2026  \nCopyright: © 2026 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license.  \n1 Second Department of Cardiology, Hippokration General Hospital, Aristotle University of Thessaloniki, Konstantinoupoleos 49, 54642 Thessaloniki, Greece; [aantoniadis@gmail.com](aantoniadis@gmail.com) (A.P.A.); [fragakis.nikos@gmail.com](fragakis.nikos@gmail.com) (N.F.)  \n2 First Cardiology Department, School of Medicine, Hippokration General Hospital, National and Kapodistrian University of Athens, 10679 Athens, Greece; [panayiotisiliakis@gmail.com](panayiotisiliakis@gmail.com)  \n3 Department of Cardiology, Georgios Papanikolaou General Hospital, Leoforos Papanikolaou,  \n57010 Thessaloniki, Greece; [sidiropoulos.georges@gmail.com](sidiropoulos.georges@gmail.com)  \n4 Department of Pharmacology, University of Athens, 75 Mikras Asias Avenue, 11527 Goudi, Greece; [dinosgrigoriou@gmail.com](dinosgrigoriou@gmail.com)  \n5 Second Propedeutic Department of Internal Medicine, Faculty of Medicine, School of Health Sciences Aristotle, University of Thessaloniki, 54642 Thessaloniki, Greece; [dipatoulias@gmail.com](dipatoulias@gmail.com)  \n* [Correspondence: pakar15@hotmail.com](Correspondence: pakar15@hotmail.com)  \nAbstract  \nObesity-associated inflammation underlies much of cardiometabolic pathology, reflecting the convergence of chronic, low-grade systemic immune activation with region-specific maladaptation of adipose depots. Among these, epicardial adipose tissue (EAT)—a visceral fat layer contiguous with the myocardium and sharing its microvasculature—functions as a cardio-proximal immunometabolic interface that influences atrial fibrillation, heart failure with preserved ejection fraction, and coronary atherogenesis through paracrine crosstalk. These relationships extend beyond crude measures of adiposity, emphasizing the primacy of local inflammatory signaling, adipokine flux, and fibro-inflammatory remodeling at the EAT–myocardium interface. Of importance, substantial weight reduction only partially reverses obesity-imprinted transcriptional and epigenetic programs across subcutaneous, visceral, and epicardial depots, supporting the concept of an enduring adipose memory that sustains cardiovascular (CV) risk despite metabolic improvement. Accordingly, therapeutic strategies should move beyond weight-centric management toward mechanism-guided interventions. Resolution pharmacology—leveraging specialized pro-resolving mediatorsand their cognate G-protein-coupled receptors—offers a biologically plausible means to terminate inflammation and reprogram immune–stromal interactions within adipose and CV tissues. Although preclinical studies report favorable effects on vascular remodeling, myocardial injury, and arrhythmic vulnerability, clinical translation is constrained by pharmacokinetic liabilities of native mediators and by incomplete validation of biomarkers for target engagement. This review integrates mechanistic, depot-resolved, and therapeutic evidence to inform the design of next-generation anti-inflammatory strategies for obesityrelated CV disease.  \nKeywords: obesity; inflammation; resolution pharmacology; heart failure; atrial fibrillation; coronary artery disease; adipokines  \n1. Introduction  \nInflammation is fundamentally protective, containing and eliminating threats to the host [1] . Yet when termination fails or is delayed, an initially adaptive program hardens into chronic, low-grade activation that","cbCaioOrMcsgbiov","https://ap.wps.com/l/cbCaioOrMcsgbiov","pdf",1636800,29,"English","# Abstract\n# Introduction\n# Scope and Literature Search","[{\"question\":\"How does resolution pharmacology differ from weight-centric approaches?\",\"answer\":\"Resolution pharmacology targets endogenous active resolution pathways using specialized pro-resolving mediators and their cognate receptors to terminate inflammation and reprogram immune–stromal interactions without broad immunosuppression. The review emphasizes moving beyond weight-centric management toward mechanism-guided interventions.\"}]","Inflammation and Resolution in Obesity-Related Cardiovascular Disease | PDF",1790764411,73]