Zhong Yi-Lang, Xu Chen-Qin, Li Ji, Liang Zhi-Qiang, Wang Miao-Miao, Ma Chao, Jia Cheng-Lin, Cao Yong-Bing, Chen Jian
Institute of Vascular Anomalies, Shanghai TCM-Integrated Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200082, China.
Department of Vascular Disease, Shanghai TCM-Integrated Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200082, China.
Phytomedicine. 2025 May;140:156620. doi: 10.1016/j.phymed.2025.156620. Epub 2025 Mar 7.
Mitochondria regulate macrophage function, affecting cardiovascular diseases like atherosclerosis and heart failure. Their dynamics interact with macrophage cell death mechanisms, including apoptosis and necroptosis.
This review explores how mitochondrial dynamics and metabolism influence macrophage inflammation and cell death in CVDs, highlighting therapeutic targets for enhancing macrophage resilience and reducing CVD pathology, while examining molecular pathways and pharmacological agents involved.
This is a narrative review that integrates findings from various studies on mitochondrial dynamics and metabolism in macrophages, their interactions with the endoplasmic reticulum (ER) and Golgi apparatus, and their implications for CVDs. The review also considers the potential therapeutic effects of pharmacological agents on these pathways.
The review utilizes a comprehensive literature search to identify relevant studies on mitochondrial dynamics and metabolism in macrophages, their role in CVDs, and the effects of pharmacological agents on these pathways. The selected studies are analyzed and synthesized to provide insights into the complex relationships between mitochondria, the ER, and Golgi apparatus, and their implications for macrophage function and fate.
The review reveals that mitochondrial metabolism intertwines with cellular architecture and function, particularly through its intricate interactions with the ER and Golgi apparatus. Mitochondrial-associated membranes (MAMs) facilitate Ca2+ transfer from the ER to mitochondria, maintaining mitochondrial homeostasis during ER stress. The Golgi apparatus transports proteins crucial for inflammatory signaling, contributing to immune responses. Inflammation-induced metabolic reprogramming in macrophages, characterized by a shift from oxidative phosphorylation to glycolysis, underscores the multifaceted role of mitochondrial metabolism in regulating immune cell polarization and inflammatory outcomes. Notably, mitochondrial dysfunction, marked by heightened reactive oxygen species generation, fuels inflammatory cascades and promotes cell death, exacerbating CVD pathology. However, pharmacological agents such as Metformin, Nitazoxanide, and Galanin emerge as potential therapeutic modulators of these pathways, offering avenues for mitigating CVD progression.
This review highlights mitochondrial dynamics and metabolism in macrophage inflammation and cell death in CVDs, suggesting therapeutic targets to improve macrophage resilience and reduce pathology, with new pharmacological agents offering treatment opportunities.
线粒体调节巨噬细胞功能，影响动脉粥样硬化和心力衰竭等心血管疾病。其动力学与巨噬细胞细胞死亡机制相互作用，包括凋亡和坏死性凋亡。
本综述探讨线粒体动力学和代谢如何影响心血管疾病中巨噬细胞的炎症和细胞死亡，强调增强巨噬细胞恢复力和减轻心血管疾病病理的治疗靶点，同时研究相关分子途径和药物。
这是一篇叙述性综述，整合了关于巨噬细胞中线粒体动力学和代谢、它们与内质网（ER）和高尔基体的相互作用及其对心血管疾病影响的各种研究结果。该综述还考虑了药物对这些途径的潜在治疗作用。
本综述通过全面的文献检索，确定关于巨噬细胞中线粒体动力学和代谢、它们在心血管疾病中的作用以及药物对这些途径影响的相关研究。对所选研究进行分析和综合，以深入了解线粒体、内质网和高尔基体之间的复杂关系及其对巨噬细胞功能和命运的影响。
该综述表明，线粒体代谢与细胞结构和功能相互交织，特别是通过其与内质网和高尔基体的复杂相互作用。线粒体相关膜（MAMs）促进Ca2+从内质网转移到线粒体，在内质网应激期间维持线粒体稳态。高尔基体运输对炎症信号传导至关重要的蛋白质，促进免疫反应。巨噬细胞中炎症诱导的代谢重编程，其特征是从氧化磷酸化转变为糖酵解，突显了线粒体代谢在调节免疫细胞极化和炎症结果方面的多方面作用。值得注意的是，以活性氧生成增加为特征的线粒体功能障碍会引发炎症级联反应并促进细胞死亡，加剧心血管疾病病理。然而，二甲双胍、硝唑尼特和甘丙肽等药物成为这些途径的潜在治疗调节剂，为减轻心血管疾病进展提供了途径。
本综述强调了心血管疾病中巨噬细胞炎症和细胞死亡中的线粒体动力学和代谢，提出了改善巨噬细胞恢复力和减轻病理的治疗靶点，新的药物提供了治疗机会。
