ArticleInternational journal of molecular sciences2018
Endogenous Selenoprotein P, a Liver-Derived Secretory Protein, Mediates Myocardial Ischemia/Reperfusion Injury in Mice.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Effects of eicosapentaenoic acid on serum levels of selenoprotein P and organ-specific insulin sensitivity in humans with dyslipidemia and type 2 diabetes.Journal of diabetes investigation · 2022Trial
- Selenoprotein P deficiency in MASLD: association with insulin resistance and liver fibrosis: a prospective case-control study.BMC gastroenterology · 2026Article
- Link between Metabolic Dysfunction-Associated Steatotic Liver Disease and Cardiovascular Diseases.Research (Washington, D.C.) · 2026Review
- Selenium and selenoproteins in age-related metabolic diseases: mechanistic insights and translational perspectives.Frontiers in nutrition · 2026Review
- Hepatic Mechanisms of Myocardial Infarction: A New Perspective in Metabolic Dysfunction-Associated Fatty Liver Disease.Journal of the American Heart Association · 2025Review
- Emerging Evidence Linking the Liver to the Cardiovascular System: Liver-derived Secretory Factors.Journal of clinical and translational hepatology · 2023Review
- Cardiac Hepatopathy: New Perspectives on Old Problems through a Prism of Endogenous Metabolic Regulations by Hepatokines.Antioxidants (Basel, Switzerland) · 2023Review
- Increases in Hepatokine Selenoprotein P Levels Are Associated With Hepatic Hypoperfusion and Predict Adverse Prognosis in Patients With Heart Failure.Journal of the American Heart Association · 2022Observational
- The Impact of Selenium Deficiency on Cardiovascular Function.International journal of molecular sciences · 2021Review
- Selenium, a Micronutrient That Modulates Cardiovascular Health via Redox Enzymology.Nutrients · 2021Review
- Hepatocardiac or Cardiohepatic Interaction: From Traditional Chinese Medicine to Western Medicine.Evidence-based complementary and alternative medicine : eCAM · 2021Review
- Alcohol Intake Is Associated With Elevated Serum Levels of Selenium and Selenoprotein P in Humans.Frontiers in nutrition · 2021Article
- Hepatokine Selenoprotein P-Mediated Reductive Stress Causes Resistance to Intracellular Signal Transduction.Antioxidants & redox signaling · 2020Review
- China Tongxinluo Study for myocardial protection in patients with Acute Myocardial Infarction (CTS-AMI): Rationale and design of a randomized, double-blind, placebo-controlled, multicenter clinical trial.American heart journal · 2020Article
- Inhibition of CLU4A exhibits a cardioprotective role in hypoxia/reoxygenation-induced injury by an ERK-dependent pathway.International journal of clinical and experimental pathology · 2019Article
- Molecular Mechanisms and Pathophysiology of Ischemia-Reperfusion Injury.International journal of molecular sciences · 2018Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selenoprotein P (SeP), a liver-derived secretory protein, functions as a selenium supply protein in the body. SeP has been reported to be associated with insulin resistance in humans through serial analysis of gene expression. Recently, SeP has been found to inhibit vascular endothelial growth factor-stimulated cell proliferation in human umbilical vein endothelial cells, and impair angiogenesis in a mouse hind limb model. In this study, the role of SeP in ischemia/reperfusion (I/R) injury has been investigated. SeP knockout (KO) and littermate wild-type (WT) mice were subjected to 30 min of myocardial ischemia followed by 24 h of reperfusion. The myocardial infarct area/area at risk (IA/AAR), evaluated using Evans blue (EB) and 2,3,5-triphenyltetrazolium chloride (TTC) staining, was significantly smaller in SeP KO mice than in WT mice. The number of terminal de-oxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive nuclei was significantly lower in SeP KO mice than in WT mice. In addition, caspase-3 activation was reduced in SeP KO mice compared to that in WT mice. Furthermore, phosphoinositide 3-kinase/Akt and Erk levels were examined for the reperfusion injury salvage kinase (RISK) pathway. Interestingly, SeP KO significantly increased the phosphorylation of IGF-1, Akt, and Erk compared to that in WT mice after I/R. Finally, I/R-induced myocardial IA/AAR was significantly increased in SeP KO mice overexpressing SeP in the liver compared to other SeP KO mice. These results, together, suggest that inhibition of SeP protects the heart from I/R injury through upregulation of the RISK pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.