From Bench to Clinic: Advances in Anti-Inflammatory Therapies for Atherosclerotic Coronary Artery Disease

IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Kan Wang, Zheng Yin, Yang Zhang, Xianpeng Wu, Lin Fan
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Abstract

Atherosclerosis (AS) is a chronic, progressive inflammatory disorder characterized by the deposition of lipid-laden plaques, infiltration of immune cells, and remodeling of vascular structures within arterial walls. It remains the primary pathological driver of atherosclerotic coronary artery disease (ASCAD) and a major contributor to global mortality. While conventional lipid-lowering therapies, particularly statins, have significantly reduced the incidence of ASCAD by targeting hyperlipidemia, a considerable residual inflammatory risk continues to exist. This unresolved inflammation exacerbates plaque vulnerability, increases the likelihood of rupture, and precipitates thrombotic complications. Recent breakthroughs in understanding the complex inflammatory mechanisms underlying AS, including endothelial dysfunction, macrophage polarization, T-cell activation, and the release of pro-inflammatory cytokines, have revealed novel therapeutic targets. This mechanistic insight has spurred the development of innovative anti-inflammatory strategies, including monoclonal antibodies targeting specific cytokines (e.g., IL-1β, TNF-α), epigenetic modulators, and immune-based interventions. This review synthesizes the current understanding of the inflammatory pathogenesis of AS, evaluates the translational potential of emerging anti-inflammatory therapies, and discusses the challenges in optimizing the balance between efficacy and safety. By bridging discoveries in basic science with clinical applicability, this analysis aims to guide future research and foster therapeutic innovations in combating ASCAD.

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从实验室到临床:动脉粥样硬化性冠状动脉疾病的抗炎治疗进展。
动脉粥样硬化(AS)是一种慢性进行性炎症性疾病,其特征是脂质斑块沉积、免疫细胞浸润和动脉壁内血管结构重塑。它仍然是动脉粥样硬化性冠状动脉疾病(ASCAD)的主要病理驱动因素,也是全球死亡率的主要因素。虽然传统的降脂疗法,特别是他汀类药物,通过靶向高脂血症显著降低了ASCAD的发病率,但仍然存在相当大的残余炎症风险。这种未解决的炎症加剧了斑块的易感性,增加了破裂的可能性,并引发血栓并发症。最近在了解AS的复杂炎症机制方面的突破,包括内皮功能障碍、巨噬细胞极化、t细胞活化和促炎细胞因子的释放,揭示了新的治疗靶点。这种机制的洞察力刺激了创新抗炎策略的发展,包括针对特定细胞因子的单克隆抗体(例如,IL-1β, TNF-α),表观遗传调节剂和基于免疫的干预措施。本文综述了目前对AS炎症发病机制的理解,评估了新兴抗炎疗法的转化潜力,并讨论了优化疗效和安全性之间平衡的挑战。通过将基础科学的发现与临床应用相结合,本分析旨在指导未来的研究并促进对抗ASCAD的治疗创新。
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
The FASEB Journal
The FASEB Journal 生物-生化与分子生物学
CiteScore
9.20
自引率
2.10%
发文量
6243
审稿时长
3 months
期刊介绍: The FASEB Journal publishes international, transdisciplinary research covering all fields of biology at every level of organization: atomic, molecular, cell, tissue, organ, organismic and population. While the journal strives to include research that cuts across the biological sciences, it also considers submissions that lie within one field, but may have implications for other fields as well. The journal seeks to publish basic and translational research, but also welcomes reports of pre-clinical and early clinical research. In addition to research, review, and hypothesis submissions, The FASEB Journal also seeks perspectives, commentaries, book reviews, and similar content related to the life sciences in its Up Front section.
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