ArticleMolecular and cellular biochemistry2016
Vascular endothelial growth factor-C protects heart from ischemia/reperfusion injury by inhibiting cardiomyocyte apoptosis.
Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Targeted drug delivery systems for cardiovascular disease treatment: principles, targeting strategies, and future prospects.Annals of medicine · 2026Review
- Shuxuening injection improves ventricular remodeling after myocardial infarction by indirectly promoting macrophage-mediated angiogenesis and lymphangiogenesis.Chinese medicine · 2026Article
- Vascular endothelial growth factor signaling in health and disease: from molecular mechanisms to therapeutic perspectives.Signal transduction and targeted therapy · 2025Review
- sVEGFR3 alleviates myocardial ischemia/reperfusion injury through regulating mitochondrial homeostasis and immune cell infiltration.Apoptosis : an international journal on programmed cell death · 2025Article
- Current Status of Lymphangiogenesis: Molecular Mechanism, Immune Tolerance, and Application Prospect.Cancers · 2023Review
- Network pharmacology-based analysis of potential mechanisms of myocardial ischemia-reperfusion injury by total salvianolic acid injection.Frontiers in pharmacology · 2023Review
- Immune-metabolic mechanisms of post-traumatic stress disorder and atherosclerosis.Frontiers in physiology · 2023Review
- Heart Failure And Type 2 Diabetes Mellitus: Neurohumoral, Histological And Molecular Interconnections.Current cardiology reviews · 2023Review
- The role of lymphangiogenesis in cardiovascular diseases and heart transplantation.Heart failure reviews · 2022Review
- Adenine Nucleotide Translocase 1 Expression Modulates the Immune Response in Ischemic Hearts.Cells · 2021Article
- The Role of the VEGF Family in Coronary Heart Disease.Frontiers in cardiovascular medicine · 2021Review
- Cox-2 Antagonizes the Protective Effect of Sevoflurane on Hypoxia/Reoxygenation-Induced Cardiomyocyte Apoptosis through Inhibiting the Akt Pathway.Disease markers · 2021Article
- miR-140-5p mediates bevacizumab-induced cytotoxicity to cardiomyocytes by targeting theToxicology research · 2019Article
- Roles for VEGF-C/NRP-2 axis in regulating renal tubular epithelial cell survival and autophagy during serum deprivation.Cell biochemistry and function · 2019Article
- Nanomedicine for Gene Delivery for the Treatment of Cardiovascular Diseases.Current gene therapy · 2019Review
- Eplerenone pretreatment protects the myocardium against ischaemia/reperfusion injury through the phosphatidylinositol 3-kinase/Akt-dependent pathway in diabetic rats.Molecular and cellular biochemistry · 2018Article
- Rasip1 controls lymphatic vessel lumen maintenance by regulating endothelial cell junctions.Development (Cambridge, England) · 2018Article
- VEGFC/VEGFR3 Signaling Regulates Mouse Spermatogonial Cell Proliferation via the Activation of AKT/MAPK and Cyclin D1 Pathway and Mediates the Apoptosis by affecting Caspase 3/9 and Bcl-2.Cell cycle (Georgetown, Tex.) · 2018Article
- 3,5-Dicaffeoylquinic acid protects H9C2 cells against oxidative stress-induced apoptosis via activation of the PI3K/Akt signaling pathway.Food & nutrition research · 2018Article
- Eplerenone attenuates myocardial infarction in diabetic rats via modulation of the PI3K-Akt pathway and phosphorylation of GSK-3β.American journal of translational research · 2018Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
VEGF-C is a newly identified proangiogenic protein playing an important role in vascular disease and angiogenesis. However, its role in myocardial ischemia/reperfusion (I/R) injury remains unknown. The objective of this study was to determine the role and mechanism of VEGF-C in myocardial ischemia-reperfusion injury. Rat left ventricle myocardium was injected with recombinant human VEGF-C protein (0.1 or 1.0 µg/kg b.w.) 1 h prior to myocardial ischemia-reperfusion (I/R) injury. 24 h later, the myocardial infarction size, the number of TUNEL-positive cardiomyocytes, the levels of creatine kinase (CK), CK-MB, cardiac troponin, malondialdehyde (MDA) content, and apoptosis protein Bax expression were decreased, while Bcl2 and pAkt expression were increased in VEGF-C-treated myocardium as compared to the saline-treated I/R hearts. VEGF-C also improved the function of I/R-injured hearts. In the H2O2-induced H9c2 cardiomyocytes, which mimicked the I/R injury in vivo, VEGF-C pre-treatment decreased the LDH release and MDA content, blocked H2O2-induced apoptosis by inhibiting the pro-apoptotic protein Bax expression and its translocation to the mitochondrial membrane, and consequently attenuated H2O2-induced decrease of mitochondrial membrane potential and increase of cytochrome c release from mitochondria. Mechanistically, VEGF-C activated Akt signaling pathway via VEGF receptor 2, leading to a blockade of Bax expression and mitochondrial membrane translocation and thus protected cardiomyocyte from H2O2-induced activation of intrinsic apoptotic pathway. VEGF-C exerts its cardiac protection following I/R injury via its anti-apoptotic effect.
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