Pioneering therapies for post-infarction angiogenesis: Insight into molecular mechanisms and preclinical studies
Acute myocardial infarction (MI), despite significant progress in its treatment, remains a leading cause of chronic heart failure and cardiovascular events such as cardiac arrest. Promoting angiogenesis in the myocardial tissue after MI to restore blood flow in the ischemic and hypoxic tissue is con...
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Published in | Biomedicine & pharmacotherapy Vol. 166; p. 115306 |
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Language | English |
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01.10.2023
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Abstract | Acute myocardial infarction (MI), despite significant progress in its treatment, remains a leading cause of chronic heart failure and cardiovascular events such as cardiac arrest. Promoting angiogenesis in the myocardial tissue after MI to restore blood flow in the ischemic and hypoxic tissue is considered an effective treatment strategy. The repair of the myocardial tissue post-MI involves a robust angiogenic response, with mechanisms involved including endothelial cell proliferation and migration, capillary growth, changes in the extracellular matrix, and stabilization of pericytes for neovascularization. In this review, we provide a detailed overview of six key pathways in angiogenesis post-MI: the PI3K/Akt/mTOR signaling pathway, the Notch signaling pathway, the Wnt/β-catenin signaling pathway, the Hippo signaling pathway, the Sonic Hedgehog signaling pathway, and the JAK/STAT signaling pathway. We also discuss novel therapeutic approaches targeting these pathways, including drug therapy, gene therapy, protein therapy, cell therapy, and extracellular vesicle therapy. A comprehensive understanding of these key pathways and their targeted therapies will aid in our understanding of the pathological and physiological mechanisms of angiogenesis after MI and the development and application of new treatment strategies.
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•Acute myocardial infarction (MI) can lead to chronic heart failure and cardiac arrest despite treatments.•This paper highlights six pathways in post-MI angiogenesis: PI3K/Akt/mTOR, Notch, Wnt/β-catenin, Hippo, Sonic Hedgehog, and JAK/STAT.•We discuss therapies targeting these pathways: drugs, genes, proteins, cells, and extracellular vesicle treatments.•Understanding these pathways and therapies helps grasp angiogenesis post-MI, guiding new treatment strategies.•Post-MI angiogenesis in myocardial tissue restores blood flow to ischemic areas, making it a key treatment strategy. |
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AbstractList | Acute myocardial infarction (MI), despite significant progress in its treatment, remains a leading cause of chronic heart failure and cardiovascular events such as cardiac arrest. Promoting angiogenesis in the myocardial tissue after MI to restore blood flow in the ischemic and hypoxic tissue is considered an effective treatment strategy. The repair of the myocardial tissue post-MI involves a robust angiogenic response, with mechanisms involved including endothelial cell proliferation and migration, capillary growth, changes in the extracellular matrix, and stabilization of pericytes for neovascularization. In this review, we provide a detailed overview of six key pathways in angiogenesis post-MI: the PI3K/Akt/mTOR signaling pathway, the Notch signaling pathway, the Wnt/β-catenin signaling pathway, the Hippo signaling pathway, the Sonic Hedgehog signaling pathway, and the JAK/STAT signaling pathway. We also discuss novel therapeutic approaches targeting these pathways, including drug therapy, gene therapy, protein therapy, cell therapy, and extracellular vesicle therapy. A comprehensive understanding of these key pathways and their targeted therapies will aid in our understanding of the pathological and physiological mechanisms of angiogenesis after MI and the development and application of new treatment strategies. Acute myocardial infarction (MI), despite significant progress in its treatment, remains a leading cause of chronic heart failure and cardiovascular events such as cardiac arrest. Promoting angiogenesis in the myocardial tissue after MI to restore blood flow in the ischemic and hypoxic tissue is considered an effective treatment strategy. The repair of the myocardial tissue post-MI involves a robust angiogenic response, with mechanisms involved including endothelial cell proliferation and migration, capillary growth, changes in the extracellular matrix, and stabilization of pericytes for neovascularization. In this review, we provide a detailed overview of six key pathways in angiogenesis post-MI: the PI3K/Akt/mTOR signaling pathway, the Notch signaling pathway, the Wnt/β-catenin signaling pathway, the Hippo signaling pathway, the Sonic Hedgehog signaling pathway, and the JAK/STAT signaling pathway. We also discuss novel therapeutic approaches targeting these pathways, including drug therapy, gene therapy, protein therapy, cell therapy, and extracellular vesicle therapy. A comprehensive understanding of these key pathways and their targeted therapies will aid in our understanding of the pathological and physiological mechanisms of angiogenesis after MI and the development and application of new treatment strategies. [Display omitted] •Acute myocardial infarction (MI) can lead to chronic heart failure and cardiac arrest despite treatments.•This paper highlights six pathways in post-MI angiogenesis: PI3K/Akt/mTOR, Notch, Wnt/β-catenin, Hippo, Sonic Hedgehog, and JAK/STAT.•We discuss therapies targeting these pathways: drugs, genes, proteins, cells, and extracellular vesicle treatments.•Understanding these pathways and therapies helps grasp angiogenesis post-MI, guiding new treatment strategies.•Post-MI angiogenesis in myocardial tissue restores blood flow to ischemic areas, making it a key treatment strategy. |
ArticleNumber | 115306 |
Author | Hu, Jun Liu, Chao Liu, Lanchun Chen, Cong Wang, Jie |
Author_xml | – sequence: 1 givenname: Cong surname: Chen fullname: Chen, Cong organization: Guang’anmen Hospital, China Academy of Chinese Medicine Sciences, Beijing 100053, China – sequence: 2 givenname: Jie surname: Wang fullname: Wang, Jie email: wangjie0103@126.com organization: Guang’anmen Hospital, China Academy of Chinese Medicine Sciences, Beijing 100053, China – sequence: 3 givenname: Chao surname: Liu fullname: Liu, Chao organization: Guang’anmen Hospital, China Academy of Chinese Medicine Sciences, Beijing 100053, China – sequence: 4 givenname: Jun surname: Hu fullname: Hu, Jun organization: Guang’anmen Hospital, China Academy of Chinese Medicine Sciences, Beijing 100053, China – sequence: 5 givenname: Lanchun surname: Liu fullname: Liu, Lanchun organization: Guang’anmen Hospital, China Academy of Chinese Medicine Sciences, Beijing 100053, China |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37572633$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1016_j_bbrc_2024_149941 |
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Keywords | Extracellular Vesicle Therapy Therapeutic Approaches Signaling Pathways Cardiovascular Events Post-Infarction Angiogenesis |
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