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Metabolic syndrome and cardiovascular diseases: Going beyond traditional risk factors

氧化应激 医学 代谢综合征 胰岛素抵抗 内皮功能障碍 糖尿病 炎症 腹部肥胖 疾病 内分泌学 内科学 生物信息学 风险因素 生理学 免疫学 生物
作者
João Leonardo Silveira Rossi,Sandra Maria Barbalho,Renan Reverete de Araújo,Marcelo Dib Bechara,Kátia Portero Sloan,Lance Sloan
出处
期刊:Diabetes-metabolism Research and Reviews [Wiley]
卷期号:38 (3) 被引量:330
标识
DOI:10.1002/dmrr.3502
摘要

Metabolic syndrome (MS) is a chronic non-infective syndrome characterised clinically by a set of vascular risk factors that include insulin resistance, hypertension, abdominal obesity, impaired glucose metabolism, and dyslipidaemia. These risk factors are due to a pro-inflammatory state, oxidative stress, haemodynamic dysfunction, and ischaemia, which overlap in 'dysmetabolic' patients. This review aimed to evaluate the relationship between the traditional components of MS with cardiovascular disease (CVD), inflammation, and oxidative stress. MEDLINE-PubMed, EMBASE, and Cochrane databases were searched. Chronic low-grade inflammatory states and metaflammation are often accompanied by metabolic changes directly related to CVD incidence, such as diabetes mellitus, hypertension, and obesity. Moreover, the metaflammation is characterised by an increase in the serum concentration of pro-inflammatory cytokines, mainly interleukin-1 β (IL-1β), IL-6, and tumour necrosis factor-α (TNF-α), originating from the chronically inflamed adipose tissue and associated with oxidative stress. The increase of reactive oxygen species overloads the antioxidant systems causing post-translational alterations of proteins, lipids, and DNA leading to oxidative stress. Hyperglycaemia contributes to the increase in oxidative stress and the production of advanced glycosylation end products (AGEs) which are related to cellular and molecular dysfunction. Oxidative stress and inflammation are associated with cellular senescence and CVD. CVD should not be seen only as being triggered by classical MS risk factors. Atherosclerosis is a multifactorial pathological process with several triggering and aetiopathogenic mechanisms. Its medium and long-term repercussions, however, invariably constitute a significant cause of morbidity and mortality. Implementing preventive and therapeutic measures against oxy-reductive imbalances and metaflammation states has unquestionable potential for favourable clinical outcomes in cardiovascular medicine.
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