ArticleExperimental and therapeutic medicine2022
miR-340-5p inhibits pancreatic acinar cell inflammation and apoptosis via targeted inhibition of HMGB1.
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Article
- Dysregulation of LINC01094 is involved in the pathogenesis of pulpitis by regulating the miR-340-5p expression.Odontology · 2025Article
- HMGB1: key mediator in digestive system diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Oxidative stress, DAMPs, and immune cells in acute pancreatitis: molecular mechanisms and therapeutic prospects.Frontiers in immunology · 2025Review
- Damage associated molecular patterns and neutrophil extracellular traps in acute pancreatitis.Frontiers in cellular and infection microbiology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute pancreatitis (AP) is a common gastrointestinal disease that affects 1 million individuals worldwide. Inflammation and apoptosis are considered to be important pathogenic mechanisms of AP, and high mobility group box 1 (HMGB1) has been shown to play a particularly important role in the etiology of this disease. MicroRNAs (miRs) are emerging as critical regulators of gene expression and, as such, they represent a promising area of therapeutic target identification and development for a variety of diseases, including AP. Using the online database query (microRNA.org), the current study identified a site in the 3' untranslated region of HMGB1 mRNA that was a viable target for miR-340-5p. The present study aimed to investigate the association between miR-340-5p and HMGB1 expression in pancreatic acinar cells following lipopolysaccharide (LPS) treatment by performing luciferase, western blotting and reverse transcription-quantitative PCR assays. The results suggest that miR-340-5p attenuates the induction of HMGB1 by LPS, thereby inhibiting inflammation and apoptosis via blunted activation of Toll-like receptor 4 and enhanced AKT signaling. Thus, the therapeutic application of miR-340-5p may be a useful strategy in AP via upregulation of HMGB1 and subsequent promotion of inflammation and apoptosis.
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Registered trials
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