ArticleIntensive care medicine experimental2017
Myocardial oxidative stress correlates with left ventricular dysfunction on strain echocardiography in a rodent model of sepsis.
Article in Intensive care medicine experimental, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 58 citations in OpenAlex.
- Deletion of the mouse myocardial Nppb gene alleviates sepsis-induced myocardial dysfunction.Journal of molecular histology · 2026Article
- Targeting cardiac resident CCR2+ macrophage-secreted MCP-1 to attenuate inflammation after myocardial infarction.Acta biomaterialia · 2026Article
- Sepsis-Induced Cardiomyopathy and Cardiac Arrhythmias: Pathophysiology and Implications for Novel Therapeutic Approaches.Biomedicines · 2025Review
- Combatting sepsis-induced myocardial dysfunction: emerging mechanisms and immunomodulatory breakthroughs.Frontiers in immunology · 2025Review
- Impact of early myocardial injury on patients with severe pneumonia.Internal and emergency medicine · 2024Article
- Current Perspectives of Mitochondria in Sepsis-Induced Cardiomyopathy.International journal of molecular sciences · 2024Review
- Engineered exosomes: a potential therapeutic strategy for septic cardiomyopathy.Frontiers in cardiovascular medicine · 2024Review
- ALDH2 mitigates LPS-induced cardiac dysfunction, inflammation, and apoptosis through the cGAS/STING pathway.Molecular medicine (Cambridge, Mass.) · 2023Article
- Knockdown of 11β-hydroxysteroid dehydrogenase type 1 alleviates LPS-induced myocardial dysfunction through the AMPK/SIRT1/PGC-1α pathway.Journal of biomedical research · 2023Article
- Drp1/p53 interaction mediates p53 mitochondrial localization and dysfunction in septic cardiomyopathy.Journal of molecular and cellular cardiology · 2023Article
- Recombinant human angiotensin-converting enzyme 2 plays a protective role in mice with sepsis-induced cardiac dysfunction through multiple signaling pathways dependent on converting angiotensin II to angiotensin 1-7.Annals of translational medicine · 2023Article
- Research Progress on the Mechanism and Management of Septic Cardiomyopathy: A Comprehensive Review.Emergency medicine international · 2023Review
- Sex-specific differences in cardiac function, inflammation and injury during early polymicrobial sepsis.Intensive care medicine experimental · 2022Article
- Roles of neutrophil reactive oxygen species (ROS) generation in organ function impairment in sepsis.Journal of Zhejiang University. Science. B · 2022Review
- Red Blood Cell Membrane-Camouflaged PLGA Nanoparticles Loaded With Basic Fibroblast Growth Factor for Attenuating Sepsis-Induced Cardiac Injury.Frontiers in pharmacology · 2022Article
- Cardiac Metabolism in Sepsis.Metabolites · 2021Review
- Left ventricular global longitudinal strain in low cardiac risk outpatients who recently recovered from coronavirus disease 2019.The international journal of cardiovascular imaging · 2021Article
- Early Vitamin C, Hydrocortisone, and Thiamine Treatment for Septic Cardiomyopathy: A Propensity Score Analysis.Journal of personalized medicine · 2021Article
- Pathophysiology of sepsis-induced cardiomyopathy.Nature reviews. Cardiology · 2021Review
- Regulatory role of the TLR4/JNK signaling pathway in sepsis‑induced myocardial dysfunction.Molecular medicine reports · 2021Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
backgroundRecognition of cardiomyopathy in sepsis can be challenging due to the limitations of conventional measures such as ejection fraction (EF) and fractional shortening (FS) in the context of variable preload and afterload conditions. This study correlates myocardial function using strain echocardiography (SE) with cardiomyocyte oxidative stress in a murine model of sepsis.
methodsC57BL/6J mice were randomized into control (n = 10), sham (n = 25), and a cecal ligation and puncture (CLP) (n = 33) model of sepsis. Echocardiography was performed pre-, 12, 24, and 48 h post-injury. Cardiac pro-inflammatory cytokines and mitochondrial redox scavenger expression were evaluated in a subset of each arm. To evaluate the influence of redox scavenger upregulation on oxidative injury and cardiac function, CLP was performed on mitochondrial catalase-upregulated C57BL/6J MCAT
resultsSeptic C57BL/6J mice exhibited depressed longitudinal strain (LS) when compared to sham and control at 24 h (p < 0.01) and 48 h (p = 0.04) post-CLP despite having a preserved EF. Furthermore, there was a significant association between increased odds of mortality and depressed LS (OR = 1.23, p = 0.04). Septic C57BL/6J mice concomitantly demonstrated increased expression of cardiomyocyte pro-inflammatory cytokines and decreased expression of redox scavengers at 24 and 48 h. When comparing C57Bl/6 MCAT
conclusionsIn this sepsis model, SE identified cardiomyopathy despite normal EF. SE depression temporally coincides with upregulation of inflammatory cytokines and decreases expression of key mitochondrial ROS scavengers. Upregulation of redox scavenger (CAT) abrogates oxidative stress and cardiac dysfunction in this sepsis model.
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