On the Role of Paraoxonase-1 and Chemokine Ligand 2 (C-C motif) in Metabolic Alterations Linked to Inflammation and Disease. A 2021 Update.
On the Role of Paraoxonase-1 and Chemokine Ligand 2 (C-C motif) in Metabolic Alterations Linked to Inflammation and Disease. A 2021 Update.
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DOI：
10.3390/biom11070971
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发表时间：
2021-07-01
期刊：
影响因子：
5.5
通讯作者：
Joven J
中科院分区：
文献类型：
--
作者：
Camps J;Castañé H;Rodríguez-Tomàs E;Baiges-Gaya G;Hernández-Aguilera A;Arenas M;Iftimie S;Joven J
感染性疾病和许多非感染性疾病具有共同的分子机制。其中，氧化应激和随后的炎症反应特别值得注意。由外部因素引起的代谢紊乱，无论是细菌或病毒病原体，过量的卡路里摄入，劣质营养素或环境因素，都会导致自由基和内源性抗氧化系统之间的不平衡;其结果是脂质，蛋白质和核酸的氧化。氧化和炎症密切相关，无论氧化应激和炎症是细胞病理学的原因还是结果，都产生影响疾病发病机制的代谢改变。在这篇综述中，我们强调在这些过程中的调节的两个关键分子：对氧磷酶-1（PON 1）和趋化因子（C-C基序）配体2（CCL 2）。PON 1是一种与高密度脂蛋白结合的酶。它分解脂蛋白和细胞中的脂质过氧化物，参与HDL对不同感染因子的保护，并被认为是先天免疫系统的一部分。PON 1缺乏时，CCL 2的产生增加，诱导免疫细胞在靶组织中的迁移和浸润，并干扰正常的代谢功能。这种破坏涉及控制细胞稳态的途径以及代谢驱动的慢性炎症状态。因此，了解这些关系将有助于改善治疗方法，并确定新的治疗靶点。
Infectious and many non-infectious diseases share common molecular mechanisms. Among them, oxidative stress and the subsequent inflammatory reaction are of particular note. Metabolic disorders induced by external agents, be they bacterial or viral pathogens, excessive calorie intake, poor-quality nutrients, or environmental factors produce an imbalance between the production of free radicals and endogenous antioxidant systems; the consequence being the oxidation of lipids, proteins, and nucleic acids. Oxidation and inflammation are closely related, and whether oxidative stress and inflammation represent the causes or consequences of cellular pathology, both produce metabolic alterations that influence the pathogenesis of the disease. In this review, we highlight two key molecules in the regulation of these processes: Paraoxonase-1 (PON1) and chemokine (C-C motif) ligand 2 (CCL2). PON1 is an enzyme bound to high-density lipoproteins. It breaks down lipid peroxides in lipoproteins and cells, participates in the protection conferred by HDL against different infectious agents, and is considered part of the innate immune system. With PON1 deficiency, CCL2 production increases, inducing migration and infiltration of immune cells in target tissues and disturbing normal metabolic function. This disruption involves pathways controlling cellular homeostasis as well as metabolically-driven chronic inflammatory states. Hence, an understanding of these relationships would help improve treatments and, as well, identify new therapeutic targets.
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