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Chewing the fat on an emerging target in multiple sclerosis

机译：在多发性硬化症中咀嚼肥胖的脂肪

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In this article of EBioMedicine, An Cheng and colleagues show that blocking the function of fatty acid-binding proteins (FABPs) pharmacologically, alleviates the severity of the inflammatory demyelinating neurological condition in the experimental autoimmune encephalomyelitis (EAE) mouse model [1]. Suggesting that targeting lipid metabolism may be a viable therapeutic strategy against several pathological hallmarks of multiple sclerosis (MS). To appreciate this finding, we need to examine the role of FABP and its relationship with MS. MS is a multifactorial autoimmune and neurodegenerative condition. The presence of proinflammation brought about by reactive T cells, microglia and astrocytes, oxidative stress, and mitochondrial dysfunction that perpetuate degeneration of neurons and glial cells, including oligodendrocytes, are common hallmarks of early MS. Hence, therapeutic targets that suppress proinflammatory activities by the immune cells and astrocytes and promote the remyelination capability of oligodendrocytes are priorities in MS research. Fatty acids are known to be involved in the inflammatory response, oxidative stress, and mitochondrial dysfunction (all processes relevant to MS). Moreover, myelin (a lipid-rich membrane structure) production is dependent on fatty acid synthesis made by oligodendrocytes [2]. This makes lipid metabolism modulation a key therapeutic target considering increased adiposity is a risk factor and linked to increased disability in MS. Some have postulated that inflammation in MS is a secondary consequence of dysregulated lipid metabolism.
机译：在本文的卓越医学内，一位成和同事表明，阻断脂肪酸结合蛋白（FABPS）药理学的功能，减轻了实验自身免疫脑脊髓炎（EAE）小鼠模型中炎症脱髓鞘神经功能的严重程度[1]。建议靶向脂质代谢可能是针对多发性硬化症的几种病理标志（MS）的可行治疗策略。为了理解这一发现，我们需要检查FABP的作用及其与MS的关系。 MS是一个多因素自身免疫和神经变性条件。通过反应性T细胞，微胶质细胞，氧化应激和线粒体功能障碍引起的促炎的存在，其延长神经元和胶质细胞的退化，包括少突胶质细胞，是早期MS的常见标志。因此，抑制免疫细胞和星形胶质细胞抑制促炎活性的治疗靶点，促进少突茂密细胞的核髓键性是MS研究中的优先事项。已知脂肪酸参与炎症反应，氧化应激和线粒体功能障碍（与MS相关的所有方法）。此外，髓鞘（富含脂质的膜结构）生产取决于少突胶质细胞的脂肪酸合成[2]。这使得脂质代谢调制调节考虑肥胖增加的关键治疗目标是危险因素，并与MS中的残疾增加。有些人假设MS中的炎症是脂质代谢的次要后果。

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    《EBioMedicine》 |2021年第a期|共2页
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    Chai K. Lim;

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