ArticleJournal of cellular and molecular medicine2021
M1 Macrophage exosomes MiR-21a-5p aggravates inflammatory bowel disease through decreasing E-cadherin and subsequent ILC2 activation.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
32 citing papers in PubMed, 42 citations in OpenAlex.
- Extracellular vesicles in the heart: mediators of intercellular communication in health and disease in vitro.Cell communication and signaling : CCS · 2026Review
- Ulcerative colitis: signaling pathways, therapeutic targets and interventional strategies.Signal transduction and targeted therapy · 2026Review
- Novel perspective on immune cell regulation in gastrointestinal inflammation: the role of extracellular vesicles and therapeutic prospects.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Macrophage-derived exosomes in autoimmune diseases: mechanistic insights and therapeutic implications.Immunologic research · 2025Review
- Polarized Macrophages and Their Exosomes: Implications for Autoimmune and Immune-Mediated Diseases.Biology · 2025Review
- MicroRNAs as Key Modulators of Intestinal Barrier Function: Pattern Recognition Receptors, Epithelial Junctional Complexes, and Therapeutic Approaches.Digestive diseases and sciences · 2025Review
- Extracellular vesicles derived from lung M2 macrophages enhance group 2 innate lymphoid cells function in allergic airway inflammation.Experimental & molecular medicine · 2025Article
- Macrophage exosomes mediate palmitic acid-induced metainflammation by transferring miR-3064-5p to target IκBα and activate NF-κB signaling.Journal of advanced research · 2025Article
- Role of E-cadherin in epithelial barrier dysfunction: implications for bacterial infection, inflammation, and disease pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- Article
- Role of exosomes in gastrointestinal physiology and pathophysiology.Frontiers in immunology · 2025Review
- Circulating plasma derived exosomes from systemic lupus erythematosus aggravate lupus nephritis through miR-122-5p/FOXO3-mediated macrophage activation.Journal of nanobiotechnology · 2024Article
- Cell-derived biomimetic drug delivery system for inflammatory bowel disease therapy.Materials today. Bio · 2024Review
- Emerging role of exosomes in ulcerative colitis: Targeting NOD-like receptor family pyrin domain containing 3 inflammasome.World journal of gastroenterology · 2024Review
- Article
- Macrophage-derived extracellular vesicles as new players in chronic non-communicable diseases.Frontiers in immunology · 2024Review
- Targeted delivery of budesonide in acetic acid induced colitis: impact on miR-21 and E-cadherin expression.Drug delivery and translational research · 2023Article
- Emerging functions and clinical applications of exosomal microRNAs in diseases.Non-coding RNA research · 2023Review
- Salivary Exosomes in Health and Disease: Future Prospects in the Eye.International journal of molecular sciences · 2023Review
- Exosome-mediated macrophage regulation for inflammatory bowel disease repair: a potential target of gut inflammation.American journal of translational research · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Abnormal immune regulation is a key feature of the complex pathogenic mechanism of ulcerative colitis (UC). In particular, macrophages and group 2 innate lymphoid cells (ILC2s) are important components of natural immunity that have been shown to play important roles in the pathogenesis of UC, as well as decreased E-cadherin expression on the colonic mucosa. However, it remains unclear how these components interact with each other. In this study, we investigated the molecular mechanisms of UC mediated by macrophage-derived exosomes. We showed for the first time that miR-21a-5p expression is increased in the peritoneal exosomes of mice with dextran sulphate sodium induced enteritis and that miR-21a-5p expression correlates negatively with E-cadherin expression in enterocytes. Moreover, we confirmed that miR-21a-5p was mainly derived from M1 macrophages and demonstrated that KLRG1, a surface inhibitory receptor on ILC2s, participated in excessive ILC2 activation in UC by promoting GATA-3. In conclusion, our results suggest molecular targets and provide a theoretical basis for elucidating the pathogenesis of UC and improving its treatment.
Indexed as
Identifiers
What OpenQuestion holds
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.