ArticleDiscoveries (Craiova, Romania)2017
Anti-inflammatory Gold-Induced Autologous Cytokines treatment triggers heart failure after myocardial infarction.
Article in Discoveries (Craiova, Romania), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Gold-Induced Cytokine (GOLDIC) for the Management of Knee Osteoarthritis: A Systematic Review.Cureus · 2024Review
- GOLDIC Therapy Holds Promise as an Orthobiologic Agent: A Systematic Review of the Literature.Indian journal of orthopaedics · 2024Review
- Gold-Induced Cytokine (GOLDIC®) Therapy in the Management of Knee Osteoarthritis: An Observational Study.Cureus · 2023Article
- Neutrophils Modulate Fibroblast Function and Promote Healing and Scar Formation after Murine Myocardial Infarction.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGold-induced autologous cytokine (GOLDIC) treatment is usually used in the therapy of the inflammatory musculoskeletal disorders (e.g. osteoarthritis in humans) and is able to modulate the inflammatory reaction. Moreover, governed by chemokines and cytokines, the complex inflammatory response after an acute myocardial infarction (MI), the main cause of death worldwide, plays an important role in the preservation of heart function. Therefore, we hypothesized that GOLDIC could also have an important role in ventricular remodeling after MI.
methodsMyocardial infarction was induced in mice and GOLDIC-enriched serum was directly injected directly in the infarcted tissue. Four weeks later, the function of the heart, as well as the infarction size and the scar composition were analyzed. Statistical analysis was performed with Prism 6.1 software (GraphPad), using 1-way ANOVA, followed by Newman-Keuls post-hoc-test, as indicated. Data are represented as mean ± SEM.
resultsFour weeks after MI, GOLDIC-treated mice show significantly decreased heart function and higher infarction size compared to the control group. Immunohistochemistry reveals a significantly increased number of myofibroblasts, correlating with higher collagen content in the infarcted area. Despite impaired heart function, angiogenesis in the GOLDIC-treated group is improved compared with the control, due to the increased vascular endothelial growth factor (VEGF) in the GOLDIC serum.
conclusionsIn conclusion, GOLDIC treatment impairs the ventricular remodeling, worsening the heart function. Therefore, these systemic effects should be taken into account when new therapies are designed for the musculoskeletal disorders.
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