AlZaim Ibrahim, Hammoud Safaa H, Al-Koussa Houssam, Ghazi Alaa, Eid Ali H, El-Yazbi Ahmed F
Department of Pharmacology and Toxicology, American University of Beirut, Beirut, Lebanon.
Department of Biochemistry and Molecular Genetics, American University of Beirut, Beirut, Lebanon.
Front Cardiovasc Med. 2020 Nov 17;7:602088. doi: 10.3389/fcvm.2020.602088. eCollection 2020.
Adipose tissue is a critical regulator of systemic metabolism and bodily homeostasis as it secretes a myriad of adipokines, including inflammatory and anti-inflammatory cytokines. As the main storage pool of lipids, subcutaneous and visceral adipose tissues undergo marked hypertrophy and hyperplasia in response to nutritional excess leading to hypoxia, adipokine dysregulation, and subsequent low-grade inflammation that is characterized by increased infiltration and activation of innate and adaptive immune cells. The specific localization, physiology, susceptibility to inflammation and the heterogeneity of the inflammatory cell population of each adipose depot are unique and thus dictate the possible complications of adipose tissue chronic inflammation. Several lines of evidence link visceral and particularly perivascular, pericardial, and perirenal adipose tissue inflammation to the development of metabolic syndrome, insulin resistance, type 2 diabetes and cardiovascular diseases. In addition to the implication of the immune system in the regulation of adipose tissue function, adipose tissue immune components are pivotal in detrimental or otherwise favorable adipose tissue remodeling and thermogenesis. Adipose tissue resident and infiltrating immune cells undergo metabolic and morphological adaptation based on the systemic energy status and thus a better comprehension of the metabolic regulation of immune cells in adipose tissues is pivotal to address complications of chronic adipose tissue inflammation. In this review, we discuss the role of adipose innate and adaptive immune cells across various physiological and pathophysiological states that pertain to the development or progression of cardiovascular diseases associated with metabolic disorders. Understanding such mechanisms allows for the exploitation of the adipose tissue-immune system crosstalk, exploring how the adipose immune system might be targeted as a strategy to treat cardiovascular derangements associated with metabolic dysfunctions.
脂肪组织是全身代谢和身体内环境稳态的关键调节因子,因为它能分泌大量脂肪因子,包括炎性和抗炎性细胞因子。作为脂质的主要储存库,皮下和内脏脂肪组织会因营养过剩而发生显著的肥大和增生,进而导致缺氧、脂肪因子失调,以及随后的低度炎症,其特征是固有免疫细胞和适应性免疫细胞的浸润和激活增加。每个脂肪库的特定定位、生理学、对炎症的易感性以及炎症细胞群体的异质性都是独特的,因此决定了脂肪组织慢性炎症可能产生的并发症。有多项证据表明内脏脂肪组织炎症,尤其是血管周围、心包和肾周脂肪组织炎症与代谢综合征、胰岛素抵抗、2型糖尿病和心血管疾病的发生有关。除了免疫系统在调节脂肪组织功能中的作用外,脂肪组织免疫成分在有害或有利的脂肪组织重塑和产热过程中也起着关键作用。脂肪组织中的常驻免疫细胞和浸润免疫细胞会根据全身能量状态进行代谢和形态适应,因此更好地理解脂肪组织中免疫细胞的代谢调节对于解决慢性脂肪组织炎症的并发症至关重要。在这篇综述中,我们讨论了脂肪组织固有免疫细胞和适应性免疫细胞在各种生理和病理生理状态下的作用,这些状态与代谢紊乱相关的心血管疾病的发生或发展有关。了解这些机制有助于利用脂肪组织与免疫系统的相互作用,探索如何将脂肪免疫系统作为治疗与代谢功能障碍相关的心血管紊乱的一种策略。