Inappropriate Activation of TLR4/NF-κB is a Cause of Heart Failure

IF 0.9 4区 医学 Q4 CARDIAC & CARDIOVASCULAR SYSTEMS
Jiedong Zhou, Hui Lin, Tingting Lv, Jinjin Hao, Hanlin Zhang, Shimin Sun, Juntao Yang, J. Chi, Hangyuan Guo
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引用次数: 0

Abstract

Significance: Heart failure, a disease with extremely high incidence, is closely associated with inflammation and oxidative stress. The Toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) pathway plays an important role in the occurrence and development of heart failure. Recent advances: Previous studies have shown that TLR4/NF-κB causes heart failure by inducing oxidative stress and inflammation; damaging the endothelia; promoting fibrosis; and inducing myocardial hypertrophy, apoptosis, pyroptosis, and autophagy. Critical issues: Understanding the pathogenesis of heart failure is essential for the treatment of this disease. In this review, we outline the mechanisms underlying TLR4/NF-κB pathway-mediated heart failure and discuss drugs that alleviate heart failure by regulating the TLR4/NF-κB pathway. Future directions: During TLR4/NF-κB overactivation, interventions targeting specific receptor antagonists may effectively alleviate heart failure, thus providing a basis for the development of new anti-heart failure drugs.
TLR4/NF-κB的不适当激活是心力衰竭的原因之一
意义:心力衰竭是一种发病率极高的疾病,与炎症和氧化应激密切相关。toll样受体4 (TLR4)/核因子κ b (NF-κB)通路在心力衰竭的发生发展中起重要作用。近期研究进展:已有研究表明,TLR4/NF-κB通过诱导氧化应激和炎症导致心力衰竭;破坏内皮细胞;促进纤维化;并诱导心肌肥大、凋亡、焦亡和自噬。关键问题:了解心力衰竭的发病机制对治疗此病至关重要。在这篇综述中,我们概述了TLR4/NF-κB途径介导心力衰竭的机制,并讨论了通过调节TLR4/NF-κB途径缓解心力衰竭的药物。未来发展方向:在TLR4/NF-κB过度激活过程中,针对特异性受体拮抗剂的干预可能会有效缓解心力衰竭,从而为开发新的抗心力衰竭药物提供基础。
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来源期刊
Cardiovascular Innovations and Applications
Cardiovascular Innovations and Applications CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
0.80
自引率
20.00%
发文量
222
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