ArticleExperimental biology and medicine (Maywood, N.J.)2016
Exogenous spermine inhibits hypoxia/ischemia-induced myocardial apoptosis via regulation of mitochondrial permeability transition pore and associated pathways.
Article in Experimental biology and medicine (Maywood, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Polyamine metabolism in ischemia reperfusion injury: common mitochondrial mechanisms and organ-specific differences.Journal of translational medicine · 2026Review
- Polyamine metabolism in cancer: drivers of immune evasion, ferroptosis and therapy resistance.Expert reviews in molecular medicine · 2025Review
- Spermine delivered by ZIF90 nanoparticles alleviates atherosclerosis by targeted inhibition of macrophage ferroptosis in plaque.Journal of nanobiotechnology · 2025Article
- Dysregulation of Mitochondrial Homeostasis in Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Transcutaneous Auricular Vagus Nerve Stimulation Ameliorates Preeclampsia-Induced Apoptosis of Placental Trophoblastic Cells Via Inhibiting the Mitochondrial Unfolded Protein Response.Neuroscience bulletin · 2024Article
- Elevation of spermine remodels immunosuppressive microenvironment through driving the modification of PD-L1 in hepatocellular carcinoma.Cell communication and signaling : CCS · 2022Article
- Transcriptomics Coupled to Proteomics Reveals Novel Targets for the Protective Role of Spermine in Diabetic Cardiomyopathy.Oxidative medicine and cellular longevity · 2022Article
- Involvement of Polyamines From Cardiac Mast Cells in Myocardial Remodeling Induced by Pressure Overload Through Mitochondrial Permeability Transition Pore Opening.Frontiers in cardiovascular medicine · 2022Article
- Regulating Polyamine Metabolism by miRNAs in Diabetic Cardiomyopathy.Current diabetes reports · 2021Review
- Exogenous spermine attenuates diabetic kidney injury in rats by inhibiting AMPK/mTOR signaling pathway.International journal of molecular medicine · 2021Article
- Review
- Review
- Spermine Regulates Immune and Signal Transduction Dysfunction in Diabetic Cardiomyopathy.Frontiers in endocrinology · 2021Article
- Physiopathology of the Permeability Transition Pore: Molecular Mechanisms in Human Pathology.Biomolecules · 2020Review
- Exogenous spermine attenuates rat diabetic cardiomyopathy via suppressing ROS-p53 mediated downregulation of calcium-sensitive receptor.Redox biology · 2020Article
- The Molecular and Physiological Effects of Protein-Derived Polyamines in the Intestine.Nutrients · 2020Review
- The Active Compounds of Yixin Ningshen Tablet and Their Potential Action Mechanism in Treating Coronary Heart Disease- A Network Pharmacology and Proteomics Approach.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Heme oxygenase-1 ameliorates hypoxia/reoxygenation via suppressing apoptosis and enhancing autophagy and cell proliferation though Sirt3 signaling pathway in H9c2 cells.Naunyn-Schmiedeberg's archives of pharmacology · 2019Article
- Pretreatment with Total Flavonoid Extract from Dracocephalum Moldavica L. Attenuates Ischemia Reperfusion-induced Apoptosis.Scientific reports · 2018Article
- Pyruvate enhancement of cardiac performance: Cellular mechanisms and clinical application.Experimental biology and medicine (Maywood, N.J.) · 2018Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction (MI) is associated with a high mortality rate, which is attributed to the effects of myocyte loss that occurs as a result of ischemia-induced cell death. Very few therapies can effectively prevent or delay the effects of ischemia. Polyamines (PAs) are polycations required for cell growth and division, and their use may prevent cell loss. The aim of this study was to investigate the relationship between hypoxia/ischemia (H/I)-induced cell apoptosis and PA metabolism and to investigate the ability of spermine to limit H/I injury in cardiomyocytes by blocking the mitochondrial apoptotic pathway. Neonatal rat cardiomyocytes were placed under hypoxic conditions for 24 h after being subjected to 5 μM of spermine as a pretreatment therapy. H/I induced PA catabolism, which was indicated by a 1.3-fold up-regulation of spermidine/spermine N(1)-acetyltransferase expression. Exogenous spermine significantly reduced H/I-induced cell death rate (60 ± 2 to 36 ± 2%) and apoptosis rate (42 ± 2 to 21 ± 2%); it also attenuated lactate dehyodrogenase and creatine kinase leakage (440 ± 13 and 336 ± 16 U/L to 275 ± 15 and 235 ± 13 U/L). Furthermore, it decreases calcium overload (3.8 ± 0.2 to 2.2 ± 0.1 a.u.). Moreover, spermine pretreatment remarkably decreased cytochrome c release from the mitochondria to the cytosol, lowering the expression of cleaved caspase-3 and -9. With spermine pretreatment, there was an increase in Bcl-2 levels and phosphorylation of ERK1/2, phosphoinositide 3-kinase, Akt, and GSK-3β, preserving mitochondrial membrane potential and inducing an mitochondrial permeability transition pore opening. In conclusion, H/I decreased endogenous spermine concentrations in cardiomyocytes, which ultimately induced apoptosis. The addition of exogenous spermine effectively prevented myocyte cell death.
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