ArticleFree radical biology & medicine2017
Muscle-derived extracellular superoxide dismutase inhibits endothelial activation and protects against multiple organ dysfunction syndrome in mice.
Article in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Impacts of systemic milieu on cerebrovascular and brain aging: insights from heterochronic parabiosis, blood exchange, and plasma transfer experiments.GeroScience · 2025Review
- Muscle p62 stimulates the expression of antioxidant proteins alleviating cancer cachexia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Moderate exercise-induced dynamics on key sepsis-associated signaling pathways in the liver.Critical care (London, England) · 2023Article
- Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review.Antioxidants (Basel, Switzerland) · 2022Review
- Dihydroartemisinin beneficially regulates splenic immune cell heterogeneity through the SOD3-JNK-AP-1 axis.Science China. Life sciences · 2022Article
- Physical-Exercise-Induced Antioxidant Effects on the Brain and Skeletal Muscle.Antioxidants (Basel, Switzerland) · 2022Review
- Molecular Mechanisms of Exercise and Healthspan.Cells · 2022Review
- The role of exercise in rehabilitation of discharged COVID-19 patients.Sports medicine and health science · 2021Review
- Placental superoxide dismutase 3 mediates benefits of maternal exercise on offspring health.Cell metabolism · 2021Article
- Extracellular superoxide dismutase, a molecular transducer of health benefits of exercise.Redox biology · 2020Review
- Assessment of Serum Cytokines and Oxidative Stress Markers in Elite Athletes Reveals Unique Profiles Associated With Different Sport Disciplines.Frontiers in physiology · 2020Article
- Maternal exercise training attenuates endotoxin-induced sepsis in mice offspring.Biochemistry and biophysics reports · 2018Article
- Superoxide dismutases: Dual roles in controlling ROS damage and regulating ROS signaling.The Journal of cell biology · 2018Review
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
Abstract
Multiple organ dysfunction syndrome (MODS) is a detrimental clinical complication in critically ill patients with high mortality. Emerging evidence suggests that oxidative stress and endothelial activation (induced expression of adhesion molecules) of vital organ vasculatures are key, early steps in the pathogenesis. We aimed to ascertain the role and mechanism(s) of enhanced extracellular superoxide dismutase (EcSOD) expression in skeletal muscle in protection against MODS induced by endotoxemia. We showed that EcSOD overexpressed in skeletal muscle-specific transgenic mice (TG) redistributes to other peripheral organs through the circulation and enriches at the endothelium of the vasculatures. TG mice are resistant to endotoxemia (induced by lipopolysaccharide [LPS] injection) in developing MODS with significantly reduced mortality and organ damages compared with the wild type littermates (WT). Heterogenic parabiosis between TG and WT mice conferred a significant protection to WT mice, whereas mice with R213G knock-in mutation, a human single nucleotide polymorphism leading to reduced binding EcSOD in peripheral organs, exacerbated the organ damages. Mechanistically, EcSOD inhibits vascular cell adhesion molecule 1 expression and inflammatory leukocyte adhesion to the vascular wall of vital organs, blocking an early step of the pathology in organ damage under endotoxemia. Therefore, enhanced expression of EcSOD in skeletal muscle profoundly protects against MODS by inhibiting endothelial activation and inflammatory cell adhesion, which could be a promising therapy for MODS.
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Registered trials
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 Socratic graph.