Signaling Pathways in Inflammation and Cardiovascular Diseases: An Update of Therapeutic Strategies

Ioana Cucu
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引用次数: 3

Abstract

Inflammatory processes represent a pivotal element in the development and complications of cardiovascular diseases (CVDs). Targeting these processes can lead to the alleviation of cardiomyocyte (CM) injury and the increase of reparative mechanisms. Loss of CMs from inflammation-associated cardiac diseases often results in heart failure (HF). Evidence of the crosstalk between nuclear factor-kappa B (NF-κB), Hippo, and mechanistic/mammalian target of rapamycin (mTOR) has been reported in manifold immune responses and cardiac pathologies. Since these signaling cascades regulate a broad array of biological tasks in diverse cell types, their misregulation is responsible for the pathogenesis of many cardiac and vascular disorders, including cardiomyopathies and atherosclerosis. In response to a myriad of proinflammatory cytokines, which induce reactive oxygen species (ROS) production, several molecular mechanisms are activated within the heart to inaugurate the structural remodeling of the organ. This review provides a global landscape of intricate protein–protein interaction (PPI) networks between key constituents of NF-κB, Hippo, and mTOR signaling pathways as quintessential targetable candidates for the therapy of cardiovascular and inflammation-related diseases.
炎症和心血管疾病的信号通路:治疗策略的最新进展
炎症过程是心血管疾病(cvd)发展和并发症的关键因素。靶向这些过程可以导致心肌细胞(CM)损伤的减轻和修复机制的增加。炎症相关心脏疾病引起的CMs丢失通常导致心力衰竭(HF)。核因子κB (NF-κB)、Hippo和雷帕霉素(mTOR)的机制/哺乳动物靶点之间的串音已经在多种免疫反应和心脏病理中被报道。由于这些信号级联在不同细胞类型中调节广泛的生物学任务,它们的错误调节是许多心脏和血管疾病的发病机制,包括心肌病和动脉粥样硬化。为了应对无数的促炎细胞因子,诱导活性氧(ROS)的产生,心脏内部的几个分子机制被激活,从而开启了器官的结构重塑。这篇综述提供了NF-κB、Hippo和mTOR信号通路关键成分之间复杂的蛋白-蛋白相互作用(PPI)网络的全球图景,作为治疗心血管和炎症相关疾病的典型靶向候选物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Immuno-Analyse & Biologie Specialisee
Immuno-Analyse & Biologie Specialisee 医学-医学实验技术
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审稿时长
6-12 weeks
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