当前位置: X-MOL 学术Diabetes Metab. Syndr. Obes. Targets Ther. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Effect of Leptin on Chronic Inflammatory Disorders: Insights to Therapeutic Target to Prevent Further Cardiovascular Complication
Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy ( IF 3.3 ) Pub Date : 2021-07-17 , DOI: 10.2147/dmso.s321311
Gashaw Dessie 1 , Birhanu Ayelign 2 , Yonas Akalu 3 , Tewodros Shibabaw 1 , Meseret Derbew Molla 1
Affiliation  

Abstract: In response to obesity-associated chronic inflammatory disorders, adipose tissue releases a biologically active peptide known as leptin. Leptin activates the secretion of chemical mediators, which contribute to the pathogenesis of chronic inflammatory disorders, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and psoriasis. Conversely, adiposity and obesity are the major aggravating risk factors in the pathogenesis of metabolic syndrome (MetS), including type II diabetes mellitus and obesity-associated hypertension. Elevated level of leptin in obesity-associated hypertension causes an increase in the production of aldosterone, which also results in elevation of arterial blood pressure. Hyperleptinemia is associated with the progress of the atherosclerosis through secretion of pro-inflammatory cytokines, like interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), IL-17, and other cytokines to promote inflammation. The release of those cytokines leads to chronic inflammatory disorders and obesity-associated MetS. Thus, the aberrant leptin level in both MetS and chronic inflammatory disorders also leads to the complication of cardiovascular diseases (CVD). Therapeutic target of leptin regarding its pro-inflammatory effect and dysregulated sympathetic nervous system activity may prevent further cardiovascular complication. This review mainly assesses the mechanism of leptin on the pathogenesis and further cardiovascular risk complication of chronic inflammatory disorders.

Keywords: leptin, chronic inflammatory disorders, cardiovascular


中文翻译:

瘦素对慢性炎症性疾病的影响:对预防进一步心血管并发症的治疗靶点的见解

摘要:为了应对肥胖相关的慢性炎症性疾病,脂肪组织会释放一种称为瘦素的生物活性肽。瘦素激活化学介质的分泌,这有助于慢性炎症性疾病的发病机制,如类风湿性关节炎 (RA)、系统性红斑狼疮 (SLE) 和银屑病。相反,肥胖和肥胖是代谢综合征(MetS)发病机制中的主要加重危险因素,包括 II 型糖尿病和肥胖相关的高血压。肥胖相关高血压患者的瘦素水平升高会导致醛固酮的产生增加,这也会导致动脉血压升高。高瘦素血症通过促炎细胞因子的分泌与动脉粥样硬化的进展有关,如白介素 6 (IL-6)、肿瘤坏死因子 α (TNF-α)、IL-17 和其他促进炎症的细胞因子。这些细胞因子的释放会导致慢性炎症性疾病和肥胖相关的代谢综合征。因此,MetS 和慢性炎症性疾病中的异常瘦素水平也会导致心血管疾病 (CVD) 的并发症。瘦素在促炎作用和交感神经系统活动失调方面的治疗靶点可能会预防进一步的心血管并发症。本综述主要评估瘦素在慢性炎症性疾病的发病机制和进一步心血管风险并发症中的作用机制。这些细胞因子的释放会导致慢性炎症性疾病和肥胖相关的代谢综合征。因此,MetS 和慢性炎症性疾病中的异常瘦素水平也会导致心血管疾病 (CVD) 的并发症。瘦素在促炎作用和交感神经系统活动失调方面的治疗靶点可能会预防进一步的心血管并发症。本综述主要评估瘦素在慢性炎症性疾病的发病机制和进一步心血管风险并发症中的作用机制。这些细胞因子的释放会导致慢性炎症性疾病和肥胖相关的代谢综合征。因此,MetS 和慢性炎症性疾病中的异常瘦素水平也会导致心血管疾病 (CVD) 的并发症。瘦素在促炎作用和交感神经系统活动失调方面的治疗靶点可能会预防进一步的心血管并发症。本综述主要评估瘦素在慢性炎症性疾病的发病机制和进一步心血管风险并发症中的作用机制。瘦素在促炎作用和交感神经系统活动失调方面的治疗靶点可能会预防进一步的心血管并发症。本综述主要评估瘦素在慢性炎症性疾病的发病机制和进一步心血管风险并发症中的作用机制。瘦素在促炎作用和交感神经系统活动失调方面的治疗靶点可能会预防进一步的心血管并发症。本综述主要评估瘦素在慢性炎症性疾病的发病机制和进一步心血管风险并发症中的作用机制。

关键词:瘦素,慢性炎症性疾病,心血管
更新日期:2021-07-18
down
wechat
bug