Article
Biochemistry & Molecular Biology
Manuela Montanaro, Manuel Scimeca, Lucia Anemona, Francesca Servadei, Erica Giacobbi, Rita Bonfiglio, Elena Bonanno, Nicoletta Urbano, Arnaldo Ippoliti, Giuseppe Santeusanio, Orazio Schillaci, Alessandro Mauriello
Summary: This study investigated the association among histopathologic features of carotid plaque instability, presence of micro- or macrocalcifications, expression of inflammatory biomarkers, and major risk factors. Results showed that calcifications are common in carotid plaques, with a significant difference between micro- and macrocalcifications. Microcalcifications were associated with high inflammation and instability, while macrocalcifications seemed to stabilize the plaque and were related to M2 macrophage polarization.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Immunology
Hongxia Li, Zhiqiang Cao, Lili Wang, Chang Liu, Hongkun Lin, Yuhan Tang, Ping Yao
Summary: Cardiovascular diseases are mainly caused by atherosclerosis, and macrophages play a crucial role in its progression. The polarization phenotypes and death pathways of macrophages have an impact on plaque formation and cardiovascular vulnerability.
FRONTIERS IN IMMUNOLOGY
(2022)
Review
Biochemistry & Molecular Biology
Nataliya V. Mushenkova, Nikita G. Nikiforov, Alexandra A. Melnichenko, Vladislav Kalmykov, Nikolay K. Shakhpazyan, Varvara A. Orekhova, Alexander N. Orekhov
Summary: This review discusses the functional phenotypes of intraplaque macrophages and their distinct contribution to atherosclerosis inflammation.
Article
Biochemistry & Molecular Biology
Francesco Finamore, Gabriele Nieddu, Silvia Rocchiccioli, Rita Spirito, Anna Guarino, Marilena Formato, Antonio Junior Lepedda
Summary: Proteins within different lipoprotein classes play a key role in carrying out various functions and are associated with pathological conditions such as atherosclerosis. Detailed information about the composition and structure of these lipoproteins can contribute to understanding the mechanisms of atherosclerosis.
Article
Endocrinology & Metabolism
Xiao-Xin Jiang, Weikang Bian, Yan-Rong Zhu, Zhicheng Wang, Peng Ye, Yue Gu, Hongsong Zhang, Guangfeng Zuo, Xiaobo Li, Linlin Zhu, Zhizhong Liu, Chongxiu Sun, Shao-Liang Chen, Dai-Min Zhang
Summary: Blocking the KCa3.1 channel in macrophages inhibits the development of atherosclerotic lesions in diabetic ApoE(-/-) mice fed with a high-fat diet. This inhibition is achieved by reducing the uptake of oxidized low-density lipoproteins and decreasing the expression of proinflammatory factors through the STAT3/CD36 axis. This study provides insight into a potential therapeutic target for reducing the risk of atherosclerosis in diabetic patients.
DIABETES RESEARCH AND CLINICAL PRACTICE
(2022)
Article
Food Science & Technology
Yu Wan, Lijun Mo, Haibin Huang, Lifen Mo, Wei Zhu, Wenxue Li, Guangyu Yang, Linquan Chen, Yongning Wu, Jia Song, Xingfen Yang
Summary: Chronic cadmium exposure contributes to the progression of atherosclerosis by promoting inflammation and macrophage polarization to M1 phenotype. The activation of JAK2/STAT3 pathway and up-regulation of interleukin-6 (IL-6) play important roles in this process.
FOOD AND CHEMICAL TOXICOLOGY
(2023)
Review
Cell Biology
Elmira Mahdinia, Nafiseh Shokri, Abdolkarim Talebi Taheri, Sahar Asgharzadeh, Mohammad Elahimanesh, Mohammad Najafi
Summary: This review summarizes the cellular, structural, and molecular dysfunctions involved in the formation, growth, and remodeling of atherosclerotic plaques. It discusses the recruitment, polarization, and accumulation of cells, as well as the communication between endothelial cells, macrophages, and vascular smooth muscle cells in the plaque microenvironment. Additionally, it elaborates on the structural components of plaques and the factors contributing to their rupture and erosion in the vessel.
CELL COMMUNICATION AND SIGNALING
(2023)
Review
Oncology
Qi Xiao, Rongyao Hou, Linlin Xie, Mengying Niu, Xudong Pan, Xiaoyan Zhu
Summary: Macrophages play a crucial role in the initiation, progression, and invasion of atherosclerotic plaques in atherosclerosis (AS). Metabolic reprogramming, driven by intrinsic macrophage alterations and extrinsic factors, determines macrophage function. Intrinsic mechanisms involve signal transduction pathways and metabolic enzyme activity, while extrinsic mechanisms involve lipids and cytokines in the plaque microenvironment. Targeting these pathways may alter the fate of vulnerable plaques.
CLINICAL AND TRANSLATIONAL MEDICINE
(2023)
Article
Biochemistry & Molecular Biology
Sin-Yu Chen, Yi-Zhen Chen, Yi-Jing Lee, Chung-Lin Jiang, Shao-Chun Lu, Fu-Jung Lin
Summary: Maternal hypercholesterolemia exacerbates atherosclerosis in offspring by altering macrophage development and polarization, contributing to increased macrophage burden within lesions. This study highlights the importance of epigenetic modifications in the offspring's macrophage genome as a potential mechanism for the inheritance of cardiovascular disease susceptibility from hypercholesterolemic mothers.
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
(2021)
Article
Pharmacology & Pharmacy
Haoran Liu, Suhong Wu, Hyunho Lee, Gherardo Baudo, Matteo Massaro, Aijun Zhang, Dale J. Hamilton, Elvin Blanco
Summary: The research focuses on inducing favorable metabolic phenotypes in M1 macrophages to reduce inflammatory response and prevent plaque progression by utilizing a mitochondrial transplantation strategy.
ADVANCED THERAPEUTICS
(2022)
Article
Cell Biology
Meng Duan, Hainan Chen, Linjie Yin, Xiao Zhu, Petr Novak, Yuncheng Lv, Guojun Zhao, Kai Yin
Summary: AIBP, a secreted protein, plays a pivotal role in the development of atherosclerosis. This study found that AIBP is abundantly expressed in atherosclerotic lesions and localizes in the inner membrane of mitochondria in macrophages. Deficiency of mitochondrial AIBP promotes atherosclerosis progression by causing metabolic disorders and reducing mitophagy. This leads to M1 proinflammatory macrophage polarization, further contributing to atherosclerosis development.
CELL COMMUNICATION AND SIGNALING
(2022)
Article
Medicine, Research & Experimental
Shaohong Fang, Song Sun, Hengxuan Cai, Xiaoyi Zou, Shanjie Wang, Xinran Hao, Xin Wan, Jiangtian Tian, Zhaoying Li, Zhongze He, Wei Huang, Chenchen Liang, Zhenming Zhang, Liming Yang, Jinwei Tian, Bo Yu, Bo Sun
Summary: The research suggests that serum IRGM levels may be related to plaque rupture in STEMI patients, and deficiency of IRGM/Irgm1 can increase plaque stability by suppressing macrophage apoptosis through inhibiting ROS generation and MAPK signaling transduction. Targeting IRGM may represent a new treatment strategy for the prevention and treatment of acute cardiovascular deaths caused by plaque rupture.
Review
Immunology
Jiayong Wu, Shengping He, Zhengkun Song, Sikai Chen, Xuefeng Lin, Huimei Sun, Pengyu Zhou, Qinbao Peng, Songlin Du, Shaoyi Zheng, Xiu Liu
Summary: Atherosclerosis is a chronic inflammatory disease affecting large and medium arteries, with macrophages playing a crucial role in the inflammatory response. Modulating macrophage polarization has shown potential in controlling the progression of atherosclerosis. This review explores the role of macrophage polarization in atherosclerosis and summarizes emerging therapies for its regulation.
FRONTIERS IN IMMUNOLOGY
(2023)
Article
Chemistry, Multidisciplinary
Ziyu Wu, Min Zhou, Xueting Tang, Jiaqi Zeng, Yazhou Li, Yuning Sun, Jia Huang, Lin Chen, Mimi Wan, Chun Mao
Summary: The study reports a carrier-free nanomotor that utilizes nitric oxide (NO) as a driving force to induce autophagy of macrophages and improve abnormal lipid metabolism in atherosclerosis. The nanomotor achieves precise targeting and high biological availability with the use of trehalose, L-arginine, and phosphatidylserine.
Review
Biochemistry & Molecular Biology
Lin Shen, Weiyue Chen, Jiayi Ding, Gaofeng Shu, Minjiang Chen, Zhongwei Zhao, Shuiwei Xia, Jiansong Ji
Summary: Atherosclerosis is a chronic vascular inflammatory disease, and macrophages in the plaque play a crucial role in immune response. The phenotype of plaque macrophages changes dynamically in response to the microenvironment of the plaque. Oxygen-rich microenvironment in early plaques promotes M2/alternatively activated macrophages through oxidative phosphorylation, while the hypoxic microenvironment in advanced plaques promotes M1/classically activated macrophages through anaerobic glycolysis. Additionally, angiogenesis in the adventitia of aged plaques leads to an increased proportion of M2/M1 macrophages. This review provides insights into the dynamic changes of plaque macrophages and the regulation of plaque oxygen content and immune metabolism, which may offer new targets for the treatment of atherosclerosis.