Article
Biochemistry & Molecular Biology
Maria Ortega, Tamara Molina-Garcia, Jose Gavara, Elena de Dios, Nerea Perez-Sole, Victor Marcos-Garces, Francisco J. Chorro, Cesar Rios-Navarro, Amparo Ruiz-Sauri, Vicente Bodi
Summary: This study utilizes RNA-sequencing datasets to evaluate the genes involved in post-myocardial infarction endothelial physiology and angiogenesis regulation. The results demonstrate that endothelial proliferation and apoptosis, as well as regulation of angiogenesis, occur at different time points after myocardial infarction and involve altered expression of multiple genes.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Cell Biology
Yanan Lin, Yueying Jiang, Haiyu Xian, Xiaoxiao Cai, Tao Wang
Summary: In this research, the expression of the Pi3k/Akt pathway and VEGF in OSF were investigated, and their correlation was explored. It was found that the expression of Col-I increased as OSF progressed, but was downregulated in normal and moderate to advanced OSF tissues. VEGF expression correlated positively with Pi3k and Akt expression, and targeted regulation of the Pi3k/Akt pathway can induce VEGF expression and improve ischemia, ultimately treating OSF.
CELL PROLIFERATION
(2023)
Article
Plant Sciences
Xin Han, Guoyong Zhang, Guanghong Chen, Yuting Wu, Tong Xu, Honglin Xu, Bin Liu, Yingchun Zhou
Summary: This study found that Buyang Huanwu Decoction (BYHWD) can improve myocardial infarction (MI) by promoting angiogenesis. The underlying mechanism involves the suppression of PTEN and activation of the PI3K/Akt/GSK38 signaling pathway.
JOURNAL OF ETHNOPHARMACOLOGY
(2022)
Article
Cardiac & Cardiovascular Systems
Jianqiu Pei, Lin Cai, Fang Wang, Chuansheng Xu, Shengqiang Pei, Hongwei Guo, Xiaogang Sun, Jerold Chun, Xiangfeng Cong, Weiquan Zhu, Zhe Zheng, Xi Chen
Summary: This study found that the level of lysophosphatidic acid (LPA) was increased in the peripheral blood of mice after myocardial infarction (MI), and the expression of its receptor LPA(2) was also increased in the heart. Deficiency of Lpar2 led to impaired heart function, increased scar size, and reduced vascular density. Mechanistic studies demonstrated that LPA-LPA(2) signaling promoted angiogenesis and maintained vascular homeostasis through multiple signaling pathways.
CIRCULATION RESEARCH
(2022)
Article
Cardiac & Cardiovascular Systems
Zhenkun Li, Xueyun Huo, Keyan Chen, Fenghua Yang, Weijiang Tan, Qi Zhang, Haixu Yu, Changlong Li, Deshan Zhou, Hao Chen, Baoquan Zhao, Yuan Wang, Zhenwen Chen, Xiaoyan Du
Summary: PFN2 and exosomal PFN2 promote endothelial cell (EC) proliferation, migration, and tube formation through the PI3K-PFN2-ERK axis, suggesting that exosomal PFN2 may be a valuable target in the repair of myocardial infarction (MI) injury via angiogenesis.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2022)
Review
Cardiac & Cardiovascular Systems
Xuekun Wu, Marc R. Reboll, Mortimer Korf-Klingebiel, Kai C. Wollert
Summary: The translation describes how acute myocardial infarction causes damage to the coronary microcirculation, leading to vascular disintegration and capillary rarefication in the infarct region. Tissue repair after MI involves robust angiogenic response and interactions among various cell types through secreted proteins and receptors. Macrophages and fibroblasts have emerged as major drivers of the angiogenic response after MI, while understanding the mechanism of infarct angiogenesis creates therapeutic opportunities.
CARDIOVASCULAR RESEARCH
(2021)
Article
Cell Biology
Wen-Qing Gao, Xiao-Min Hu, Qiang Zhang, Lan Yang, Xin-Ze Lv, Shuang Chen, Peng Wu, Da-Wei Duan, Yu-Heng Lang, Meng Ning, Ke-Guan Lai, Zhi-Yuan Zhang, Bin Liang, Jing-Yu Bao, Hai-Dong Wu, Tong Li
Summary: In this study, it was found that circFASTKD1 inhibits angiogenesis in vascular endothelial cells and silencing of circFASTKD1 has therapeutic effects in hypoxia by promoting angiogenesis.
Article
Biochemistry & Molecular Biology
Xiuya Li, Yilin Lian, Yukang Wu, Zihui Ye, Jiabao Feng, Yuan Zhao, Xudong Guo, Jiuhong Kang
Summary: In this study, it was found that intramyocardial delivery of plasma exosomes from neonatal mice could help repair the adult heart after acute myocardial infarction (AMI). Cardiac endothelial cells received the majority of exosomal ligands and the pro-angiogenic effect of exosomes was mediated through the recognition of cardiac endothelial cell receptors. This ligand-receptor network provides inspiration for cardiac regeneration post-MI.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Cardiac & Cardiovascular Systems
Rayane Brinck Teixeira, Melissa Pfeiffer, Peng Zhang, Ehtesham Shafique, Bonnie Rayta, Catherine Karbasiafshar, Nagib Ahsan, Frank W. Sellke, M. Ruhul Abid
Summary: Recent studies have shown that reducing mitochondrial reactive oxygen species (ROS) through the mitochondrial antioxidant MnSOD helps maintain sub-cellular ROS levels in coronary vascular endothelial cells (ECs). In this study, researchers investigated whether EC-specific mito-ROS modulation could improve the survival and proliferation of coronary ECs after a non-reperfused acute myocardial infarction (MI). They found that reducing mito-ROS in ECs improved coronary angiogenesis and cardiac function in MI, possibly through increased activation of oxidative phosphorylation (OXPHOS) in EC mitochondria.
BASIC RESEARCH IN CARDIOLOGY
(2023)
Article
Cardiac & Cardiovascular Systems
Michael Molitor, Maria T. Bayo-Jimenez, Omar Hahad, Claudius Witzler, Stefanie Finger, Venkata S. Garlapati, Sanela Rajlic, Tanja Knopp, Tabea K. Bieler, Melania Aluia, Johannes Wild, Jeremy Lagrange, Recha Blessing, Steffen Rapp, Andreas Schulz, Hartmut Kleinert, Susanne Karbach, Sebastian Steven, Wolfram Ruf, Philipp Wild, Andreas Daiber, Thomas Muenzel, Philip Wenzel
Summary: The study found that aircraft noise may have a significant impact on the development and deterioration of ischaemic heart disease. Exposure to noise before myocardial infarction (MI) can induce cardiovascular dysfunction and inflammation, leading to worsened cardiac function and increased inflammation in the vascular and cardiac tissues. The findings suggest that reducing environmental noise exposure may improve the clinical outcomes of patients with MI.
CARDIOVASCULAR RESEARCH
(2023)
Article
Biotechnology & Applied Microbiology
Xiaoting Liang, Yuelin Zhang, Fang Lin, Mimi Li, Xin Li, Yu Chen, Jing Liu, Qingshu Meng, Xiaoxue Ma, Enhao Wang, Lu Wei, Zhiying He, Huimin Fan, Xiaohui Zhou, Yue Ding, Zhongmin Liu
Summary: Direct transplantation of mitochondria derived from mesenchymal stem cells (MSC-mt) can enhance blood vessel density, inhibit cardiac remodeling and apoptosis, thus improving heart function. MSC-mt also has protective effects on endothelial cells.
BIOENGINEERING & TRANSLATIONAL MEDICINE
(2023)
Article
Biochemistry & Molecular Biology
Jeongho Park, Hyun-Ouk Kim, Kwang-Hyun Park, Myung-Bok Wie, Sun-Eun Choi, Jang-Hyuk Yun
Summary: Angiogenesis plays a crucial role in various diseases, and the Ulmus davidiana extract U60E can alleviate symptoms by inhibiting VEGF-induced angiogenesis.
Article
Peripheral Vascular Disease
Xian Wang, Changwei Wu
Summary: This study demonstrates that Tanshinone IIA improves cardiac function post-myocardial infarction by inducing angiogenesis. It is found that Tanshinone IIA regulates the miR-499-5p/PTEN signaling pathway to promote therapeutic angiogenesis.
MICROVASCULAR RESEARCH
(2022)
Article
Cardiac & Cardiovascular Systems
Yu Huang, Liangpeng Li, Hongmei Chen, Qiao Liao, Xiaoli Yang, Dezhong Yang, Xuewei Xia, Hongyong Wang, Wei Eric Wang, Lianglong Chen, Chunyu Zeng
Summary: YY1 expression in the heart was significantly stimulated following myocardial infarction. Overexpression of YY1 improved survival rate, cardiac function, scar size, and left ventricular volume in mice, while silencing YY1 had the opposite effects. YY1 alleviated cardiac apoptosis and fibrosis, promoted angiogenesis, T helper 2 cytokine production, M2 macrophage polarization, and enhanced endothelial cell tube formation and migration ability. Enhanced Akt phosphorylation and vascular endothelial growth factor production were observed in the presence of YY1 overexpression. These effects suggest YY1 as a potential therapeutic target for myocardial infarction.
JOURNAL OF THE AMERICAN HEART ASSOCIATION
(2021)
Article
Biochemistry & Molecular Biology
Daniela Lener, Maria Noflatscher, Elke Kirchmair, Axel Bauer, Johannes Holfeld, Can Gollmann-Tepekoylue, Rudolf Kirchmair, Markus Theurl
Summary: Myocardial infarction (MI) causes irreversible tissue damage and eventual heart failure. Therapeutic angiogenesis using the neuropeptide catestatin (CST) has shown to restore perfusion in a mouse hind limb ischemia model. CST promotes capillary like tube formation, cell proliferation, and protects cardiomyocytes from apoptosis, indicating its potential as a therapy for MI.