Epicardial Fat: Physiological, Pathological, and Therapeutic Implications.
Epicardial Fat: Physiological, Pathological, and Therapeutic Implications.
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DOI：
10.1155/2016/1291537
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发表时间：
2016
影响因子：
2.1
通讯作者：
Bermúdez V
中科院分区：
文献类型：
--
作者：
Salazar J;Luzardo E;Mejías JC;Rojas J;Ferreira A;Rivas-Ríos JR;Bermúdez V
心外膜脂肪在解剖学和功能上与供血血管密切相关，这就是为什么这种脂肪组织行为的任何变化都被认为是心血管疾病发展的潜在风险因素。当促炎性脂肪因子从心外膜脂肪释放时，这可导致胰岛素敏感性降低、脂联素产生减少和血管平滑肌细胞增殖增加。这些脂肪因子通过跨细胞传递或扩散从一个隔室移动到另一个隔室，因此具有调节心肌活动的能力，这种现象称为血管分泌调节。这些脂肪因子的参与产生持续的血管收缩、增加的硬度和冠状动脉壁的弱化的状态，因此有助于动脉粥样硬化斑块的形成。因此，心外膜脂肪组织增厚应被认为是心血管疾病发展的危险因素，是心血管病理学的潜在治疗靶点，也是“内分泌-心脏病学”的分子接触点。
Epicardial fat is closely related to blood supply vessels, both anatomically and functionally, which is why any change in this adipose tissue's behavior is considered a potential risk factor for cardiovascular disease development. When proinflammatory adipokines are released from the epicardial fat, this can lead to a decrease in insulin sensitivity, low adiponectin production, and an increased proliferation of vascular smooth muscle cells. These adipokines move from one compartment to another by either transcellular passing or diffusion, thus having the ability to regulate cardiac muscle activity, a phenomenon called vasocrine regulation. The participation of these adipokines generates a state of persistent vasoconstriction, increased stiffness, and weakening of the coronary wall, consequently contributing to the formation of atherosclerotic plaques. Therefore, epicardial adipose tissue thickening should be considered a risk factor in the development of cardiovascular disease, a potential therapeutic target for cardiovascular pathology and a molecular point of contact for “endocrine-cardiology.”