ArticleAmerican journal of translational research2021
17-estradiol nanoparticles influence inflammatory response of myocardial infarction possibly through downregulation of miR-302b.
Article in American journal of translational research, 2021. 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.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Estrogen signaling processes in fibroblasts: a scoping review.Frontiers in endocrinology · 2026Article
- Nanoparticles For Rescue: Innovative Therapeutic Strategy For Cardiac Repair After Myocardial Infarction.Journal of cardiovascular translational research · 2025Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
Cardiovascular death is increasing year by year, and effective treatment is a challenging clinical problem at present. The application of nano materials has pointed to a new therapeutic direction for the clinical treatment of cardiovascular diseases, and preparation of nanoparticles (NPs) with PBCA as carrier material has become a trending spot in clinical research. In this study, we observed the influence of 17-estradiol nanoparticles (17-E2-NPs) on the inflammatory response of myocardial infarction (MI) and its regulatory effect on miR-302b. First of all, we enrolled MI patients and healthy controls, and preliminarily determined that miR-302b was highly expressed in MI and positively correlated with inflammation response. Then, we prepared 17-E2-NPs and purchased rats for modeling to analyze the underlying mechanism of action. The results showed that in rats treated with 17-E2-NPs, the expression of miR-302b and inflammatory cytokines decreased, the proliferation of cardiac fibroblasts reduced and the apoptosis rate increased. According to the above results, we conclude that 17-E2-NPs can inhibit the proliferation of cardiac fibroblasts, promote the apoptosis rate and reduce the inflammatory reaction of MI, via the downregulation of miR-302b, which may be one of the effective treatment schemes for MI in the future.
Indexed as
Identifiers
34956463PMC8661167W4206862809What OpenQuestion holds
Registered trials
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