ArticleDiscoveries (Craiova, Romania)
Post-myocardial infarction treatment with resiniferatoxin modulates the expression of important genes involved in inflammation, plaque stability and angiogenesis.
Article in Discoveries (Craiova, Romania). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Space Travel: The Radiation and Microgravity Effects on the Cardiovascular System.International journal of molecular sciences · 2024Review
- Vitamin C Regulates the Profibrotic Activity of Fibroblasts in In Vitro Replica Settings of Myocardial Infarction.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ventricular tachycardia (VT) and ventricular fibrillation (VF) are the most frequent causes of death in the first 24 hours after myocardial infarction. Previous studies showed that depleting TRPV1 receptors with resiniferatoxin (RTX) led to a reduced risk of VT and VF post-myocardial infarction. Therefore, the question of resiniferatoxin as a cardioprotector against myocardial infarction (MI)-induced VT and VF was raised. The RNA sequence data from 3 groups of pigs, each having 4 animals (4 controls, 4 myocardial infarction - MI, and 4 RTX + MI) was analyzed through the lens of differentially expressed genes. The differential expression comparison was conducted in two ways: MI versus Control and RTX+MI versus MI. The results showed the downregulation of deleterious genes involved in inflammation and future plaque instability in the RTX group compared with the MI group. In the case of some of the genes, these findings were reinforced by obtaining the same trends in the MI versus Control group. All in all, we propose further investigation of RTX as a prophylactic method against cardiovascular complications of MI.
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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 OpenQuestion graph.