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瘦素在炎症中的作用及反之亦然。

Role of Leptin in Inflammation and Vice Versa.

机构信息

Department of Medical Biochemistry and Molecular Biology, and Immunology, Virgen Macarena University Hospital, University of Seville, 41009 Seville, Spain.

出版信息

Int J Mol Sci. 2020 Aug 16;21(16):5887. doi: 10.3390/ijms21165887.

Abstract

Inflammation is an essential immune response for the maintenance of tissue homeostasis. In a general sense, acute and chronic inflammation are different types of adaptive response that are called into action when other homeostatic mechanisms are insufficient. Although considerable progress has been made in understanding the cellular and molecular events that are involved in the acute inflammatory response to infection and tissue injury, the causes and mechanisms of systemic chronic inflammation are much less known. The pathogenic capacity of this type of inflammation is puzzling and represents a common link of the multifactorial diseases, such as cardiovascular diseases and type 2 diabetes. In recent years, interest has been raised by the discovery of novel mediators of inflammation, such as microRNAs and adipokines, with different effects on target tissues. In the present review, we discuss the data emerged from research of leptin in obesity as an inflammatory mediator sustaining multifactorial diseases and how this knowledge could be instrumental in the design of leptin-based manipulation strategies to help restoration of abnormal immune responses. On the other direction, chronic inflammation, either from autoimmune or infectious diseases, or impaired microbiota (dysbiosis) may impair the leptin response inducing resistance to the weight control, and therefore it may be a cause of obesity. Thus, we are reviewing the published data regarding the role of leptin in inflammation, and the other way around, the role of inflammation on the development of leptin resistance and obesity.

摘要

炎症是维持组织内稳态的必要免疫反应。一般来说,急性和慢性炎症是两种不同类型的适应性反应,当其他内稳态机制不足时,就会被激活。尽管人们在理解感染和组织损伤时急性炎症反应所涉及的细胞和分子事件方面已经取得了相当大的进展,但对系统性慢性炎症的原因和机制知之甚少。这种炎症的发病能力令人费解,它代表了多种疾病(如心血管疾病和 2 型糖尿病)的共同联系。近年来,人们对新型炎症介质(如 microRNAs 和脂肪因子)的发现产生了兴趣,这些介质对靶组织有不同的影响。在本综述中,我们讨论了肥胖症中瘦素作为维持多因素疾病的炎症介质的研究数据,以及这些知识如何有助于设计基于瘦素的干预策略,以帮助恢复异常免疫反应。另一方面,无论是自身免疫性疾病还是感染性疾病,还是受损的微生物群落(失调)引起的慢性炎症,都可能会削弱瘦素的反应,导致对体重控制的抵抗力,因此它可能是肥胖的一个原因。因此,我们正在回顾有关瘦素在炎症中的作用,以及炎症在瘦素抵抗和肥胖发展中的作用的已发表数据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f636/7460646/3a6ea6e0ebc6/ijms-21-05887-g001.jpg

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