Adipose tissue (AT) biology is linked to cardiovascular health since obesity is associated with cardiovascular disease (CVD) and positively correlated with excessive visceral fat accumulation. AT signaling to myocardial cells through soluble factors known as adipokines, cardiokines, branched-chain amino acids and small molecules like microRNAs, undoubtedly influence myocardial cells and AT function via the endocrine-paracrine mechanisms of action. Unfortunately, abnormal total and visceral adiposity can alter this harmonious signaling network, resulting in tissue hypoxia and monocyte/macrophage adipose infiltration occurring alongside expanded intra-abdominal and epicardial fat depots seen in the human obese phenotype. These processes promote an abnormal adipocyte proteomic reprogramming, whereby these cells become a source of abnormal signals, affecting vascular and myocardial tissues, leading to meta-inflammation, atrial fibrillation, coronary artery disease, heart hypertrophy, heart failure and myocardial infarction. This review first discusses the pathophysiology and consequences of adipose tissue expansion, particularly their association with meta-inflammation and microbiota dysbiosis. We also explore the precise mechanisms involved in metabolic reprogramming in AT that represent plausible causative factors for CVD. Finally, we clarify how lifestyle changes could promote improvement in myocardiocyte function in the context of changes in AT proteomics and a better gut microbiome profile to develop effective, non-pharmacologic approaches to CVD.

脂肪组织（AT）生物学与心血管健康相关，因为肥胖与心血管疾病（CVD）相关，并且与过度内脏脂肪积累呈正相关。AT 通过脂肪因子、心肌因子、支链氨基酸和小分子（如 microRNA）等可溶性因子向心肌细胞发出信号，无疑会影响心肌细胞和 AT 功能通过内分泌-旁分泌作用机制。不幸的是，异常的总体和内脏肥胖会改变这种和谐的信号网络，导致组织缺氧和单核细胞/巨噬细胞脂肪浸润，同时发生在人类肥胖表型中看到的腹内和心外膜脂肪库扩大的情况。这些过程促进异常的脂肪细胞蛋白质组重编程，从而这些细胞成为异常信号的来源，影响血管和心肌组织，导致元炎症、心房颤动、冠状动脉疾病、心脏肥大、心力衰竭和心肌梗死。这篇综述首先讨论了脂肪组织扩张的病理生理学和后果，特别是它们与后发炎症和微生物群失调的关系。我们还探索了 AT 代谢重编程中涉及的精确机制，这些机制代表了 CVD 的可能致病因素。最后，我们阐明了在 AT 蛋白质组学变化和更好的肠道微生物组概况的背景下，生活方式的改变如何促进心肌细胞功能的改善，从而开发有效的非药物治疗 CVD 方法。