ArticleAmerican journal of translational research2020
Assessment of inflammatory markers and mitochondrial factors in a rat model of sepsis-induced myocardial dysfunction.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Machine learning-based prediction of 1-year mortality risk after off-pump coronary artery bypass grafting.Journal of thoracic disease · 2026Article
- A murine model of acute and prolonged abdominal sepsis, supported by intensive care, reveals time-dependent metabolic alterations in the heart.Intensive care medicine experimental · 2025Article
- Mechanisms and Targeted Therapeutic Strategies in Sepsis-Induced Myocardial Dysfunction: The Role of NLRP3 Inflammasome-Mediated Inflammation.Journal of inflammation research · 2025Review
- Article
- Sufentanil Alleviates Sepsis-Induced Myocardial Injury and Stress Response in Rats through the ERK/GSK-3Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Kudzu Celery Decoction Exerts Protection against Sepsis-Induced Myocardial Injury.Oxidative medicine and cellular longevity · 2022Article
- Elevated Admission Cardiac Troponin I Predicts Adverse Outcomes of Acute Type B Aortic Dissection after Endovascular Treatment.Frontiers in surgery · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the expression of inflammatory markers and mitochondrial function-related genes, as well as their temporal relationship with cardiac myocyte injury in a rat model of sepsis. The sepsis model was constructed using cecal ligation and puncture (CLP). Two hours after CLP, the levels of inflammatory cytokines (interleukin [IL]-1β, IL-6, and TNFα) and myocardial function markers (serum brain natriuretic peptide [BNP], cardiac troponin-I [cTNI], and procalcitonin [PCT]) were increased significantly, falling from around 9 hours postoperatively. The concentration of nitric oxide (NO) in the heart tissue was increased 6 hours after CLP. The heart rate (HR) of rats that underwent CLP decreased 2 hours after surgery and then increased to above-normal values. The left ventricular short axis shortening (FS) and left ventricular ejection fraction (LVEF) were decreased at 2 hours postoperatively and reached a minima at 6 hours. Stroke volume (SV), cardiac output (CO), and changes and heart index (CI) results indicated myocardial dysfunction. Western blot analysis demonstrated the increased expression of mitochondrial function-related proteins and activation of mitochondrial apoptotic pathways. Hematoxylin and eosin staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays revealed that the proportion of proapoptotic cells was significantly higher in rats that underwent CLP than sham surgery at 2 to 24 hours postoperatively. Taken together, our results indicate that-in the rat model-CLP-induced sepsis leads to impaired cardiac function. Furthermore, induction of the expression of mitochondrial function-related genes indicated that myocardial cell mitochondrial function was disrupted, further aggravating cardiomyocyte apoptosis. These results provide a theoretical basis for the treatment of sepsis-induced myocardial dysfunction.
Indexed as
Identifiers
32269722PMC7137057W3018184841What OpenQuestion holds
Registered trials
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