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炎症性衰老作为自身免疫和心血管疾病之间的联系:以类风湿关节炎为例。

Inflammaging as a link between autoimmunity and cardiovascular disease: the case of rheumatoid arthritis.

机构信息

Rheumatology, Biomab IPS, Bogota, Colombia

Internal Medicine Department, Fundación Universitaria de Ciencias de la Salud (FUCS), Bogota, Cundinamarca, Colombia.

出版信息

RMD Open. 2021 Jan;7(1). doi: 10.1136/rmdopen-2020-001470.

DOI:10.1136/rmdopen-2020-001470
PMID:33468563
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7817822/
Abstract

Currently, traditional and non-traditional risk factors for cardiovascular disease have been established. The first group includes age, which constitutes one of the most important factors in the development of chronic diseases. The second group includes inflammation, the pathophysiology of which contributes to an accelerated process of vascular remodelling and atherogenesis in autoimmune diseases. Indeed, the term inflammaging has been used to refer to the inflammatory origin of ageing, explicitly due to the chronic inflammatory process associated with age (in healthy individuals). Taking this into account, it can be inferred that people with autoimmune diseases are likely to have an early acceleration of vascular ageing (vascular stiffness) as evidenced in the alteration of non-invasive cardiovascular tests such as pulse wave velocity. Thus, an association is created between autoimmunity and high morbidity and mortality rates caused by cardiovascular disease in this population group. The beneficial impact of the treatments for rheumatoid arthritis at the cardiovascular level has been reported, opening new opportunities for pharmacotherapy.

摘要

目前,心血管疾病的传统和非传统危险因素已经确定。第一组包括年龄,这是慢性病发展过程中最重要的因素之一。第二组包括炎症,其病理生理学导致自身免疫性疾病中血管重塑和动脉粥样硬化的加速过程。实际上,“炎症衰老”一词被用来指代衰老的炎症起源,明确地是由于与年龄相关的慢性炎症过程(在健康个体中)。考虑到这一点,可以推断出自身免疫性疾病患者的血管老化(血管僵硬)可能会提前加速,这在诸如脉搏波速度等非侵入性心血管测试的改变中得到了证实。因此,自身免疫与该人群心血管疾病高发病率和死亡率之间存在关联。已经报道了类风湿关节炎治疗在心血管水平上的有益影响,为药物治疗开辟了新的机会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78e7/7817822/ff8fe804425f/rmdopen-2020-001470f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78e7/7817822/536414d9e9c9/rmdopen-2020-001470f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78e7/7817822/0fed1c9743be/rmdopen-2020-001470f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78e7/7817822/ff8fe804425f/rmdopen-2020-001470f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78e7/7817822/536414d9e9c9/rmdopen-2020-001470f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78e7/7817822/0fed1c9743be/rmdopen-2020-001470f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78e7/7817822/ff8fe804425f/rmdopen-2020-001470f03.jpg

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