ArticleOpen medicine (Warsaw, Poland)2023
miR-29 regulates metabolism by inhibiting JNK-1 expression in non-obese patients with type 2 diabetes mellitus and NAFLD.
Article in Open medicine (Warsaw, Poland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.
- Impact of monotherapy and combination therapy with glucagon-like peptide-1 receptor agonists on exosomal and non-exosomal MicroRNA signatures in type 2 diabetes mellitus: a systematic review.Journal of translational medicine · 2025Pooled it
- Managing cardiovascular events, hyperglycemia, and obesity in type 2 diabetes through microRNA regulation linked to glucagon-like peptide-1 receptor agonists.Diabetology & metabolic syndrome · 2025Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that microRNAs (miRNAs) are involved in the regulation of a variety of metabolic diseases, which related to some important signal pathways. Our aim was to explore the possible mechanism of miRNAs by revealing the differential expression of serum miRNAs in different BMI of type 2 diabetes mellitus (T2DM) patients with non-alcoholic fatty liver disease (NAFLD). We found that miR-29 decreased liver aminotransferase gamma-GGT and uric acid levels by inhibiting the expression of JNK-1 in non-obese T2DM patients with NAFLD, and down-regulated the expression of atherosclerosis-related factor lipoprotein phospholipase A2 (Lp-PLA2). Combined with bioinformatics analysis, we speculate that this may be mediated by the AMPK signaling. These findings suggest that miR-29 may be a potential targeted therapeutic strategy in T2DM patients with NAFLD.
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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.