Liu Menghua, Chen Rumeng, Zheng Zhiwei, Xu Shuling, Hou Chunyan, Ding Yining, Zhang Mengling, Bao Meihua, He Binsheng, Li Sen
School of Life Sciences, Beijing University of Chinese Medicine, Beijing, China.
School of Stomatology, Changsha Medical University, Changsha, China.
Front Cardiovasc Med. 2025 Jan 14;11:1529903. doi: 10.3389/fcvm.2024.1529903. eCollection 2024.
Cardiometabolic diseases (CMD) are leading causes of death and disability worldwide, with complex pathophysiological mechanisms in which inflammation plays a crucial role. This review aims to elucidate the molecular and cellular mechanisms within the inflammatory microenvironment of atherosclerosis, hypertension and diabetic cardiomyopathy. In atherosclerosis, oxidized low-density lipoprotein (ox-LDL) and pro-inflammatory cytokines such as Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNF-α) activate immune cells contributing to foam cell formation and arterial wall thickening. Hypertension involves the activation of the renin-angiotensin system (RAS) alongside oxidative stress-induced endothelial dysfunction and local inflammation mediated by T cells. In diabetic cardiomyopathy, a high-glucose environment leads to the accumulation of advanced glycation end products (AGEs), activating the Receptor for Advanced Glycation Endproducts (RAGE) and triggering inflammatory responses that further damage cardiac and microvascular function. In summary, the inflammatory mechanisms in different types of metabolic cardiovascular diseases are complex and diverse; understanding these mechanisms deeply will aid in developing more effective individualized treatment strategies.
心血管代谢疾病（CMD）是全球死亡和残疾的主要原因，其病理生理机制复杂，炎症在其中起着关键作用。本综述旨在阐明动脉粥样硬化、高血压和糖尿病性心肌病炎症微环境中的分子和细胞机制。在动脉粥样硬化中，氧化型低密度脂蛋白（ox-LDL）以及白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）等促炎细胞因子会激活免疫细胞，导致泡沫细胞形成和动脉壁增厚。高血压涉及肾素-血管紧张素系统（RAS）的激活，同时伴有氧化应激诱导的内皮功能障碍以及由T细胞介导的局部炎症。在糖尿病性心肌病中，高糖环境会导致晚期糖基化终末产物（AGEs）的积累，激活晚期糖基化终末产物受体（RAGE）并引发炎症反应，进而进一步损害心脏和微血管功能。总之，不同类型代谢性心血管疾病中的炎症机制复杂多样；深入了解这些机制将有助于制定更有效的个体化治疗策略。
