ArticleCell metabolism2022
MiR-690 treatment causes decreased fibrosis and steatosis and restores specific Kupffer cell functions in NASH.
Article in Cell metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 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.
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Who cites it
78 citing papers in PubMed, 120 citations in OpenAlex.
- Article
- Extracellular Vesicle-Mediated Local and Systemic Communication in Metabolic Diseases.International journal of molecular sciences · 2026Review
- Urea cycle dysregulation and arginine pathways in the pathogenesis of NAFLD and NASH (Review).International journal of molecular medicine · 2026Review
- Macrophage Notch1 drives hepatocyte ferroptosis via the exosomal miR-142a-3p/TIPE2 axis to promote MASH progression.Cell & bioscience · 2026Article
- Labile iron starvation in embryonic Kupffer cells aggravates MASH via mitochondrial failure and macrophage dysfunction.Cell death & disease · 2026Article
- The OGT-TFF2 axis mediates intrahepatic crosstalk and MASH pathogenesis.Hepatology (Baltimore, Md.) · 2026Article
- The Role of Kupffer Cells and Liver Macrophages in the Pathogenesis of Metabolic Dysfunction-Associated Steatotic Liver Disease.Biomedicines · 2026Review
- Targeted Delivery of Nucleic Acid Therapeutics: Emerging Carriers and Applications in Common Metabolic and Inflammatory Diseases.International journal of nanomedicine · 2026Review
- Hepatocyte-Derived Extracellular Vesicles Deliver miR-328-3p to Trigger PP2A-B56δ-Mediated p-NLRP3Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Microbial exposure and host responses to infection reshape the disease trajectory of MASLD.Frontiers in cellular and infection microbiology · 2026Review
- The multifaceted roles of microRNAs in nonalcoholic steatohepatitis: from pathogenic mechanisms to diagnostic and therapeutic opportunities.Frontiers in genetics · 2026Review
- Role of miRNA signalling in the pathogenesis of MASLD.Frontiers in pharmacology · 2026Review
- Unlocking the benefits of aerobic exercise for MAFLD: a comprehensive mechanistic analysis.Journal of translational medicine · 2025Review
- Macrophage-derived exosomes in autoimmune diseases: mechanistic insights and therapeutic implications.Immunologic research · 2025Review
- Knowing is not enough; we must apply: the case for rigorous microRNA annotation standards.Nucleic acids research · 2025Article
- Role of Neutrophils in Homeostasis and Diseases.MedComm · 2025Review
- Regulation of Hepatic Stellate Cell Phenotypes in Metabolic Dysfunction-Associated Steatohepatitis.Gastroenterology · 2025Review
- Immunopathogenic mechanisms and immunoregulatory therapies in MASLD.Cellular & molecular immunology · 2025Review
- Extracellular vesicles in metabolic dysfunction-associated steatotic liver disease: From intercellular signaling to clinical translation.World journal of hepatology · 2025Review
- Adipose Tissue Macrophages in Metabolic Dysfunction-Associated Steatohepatitis Secrete Extracellular Vesicles That Activate Liver Fibrosis in Obese Male Mice.Gastroenterology · 2025Article
18 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Nonalcoholic steatohepatitis (NASH) is a liver disease associated with significant morbidity. Kupffer cells (KCs) produce endogenous miR-690 and, via exosome secretion, shuttle this miRNA to other liver cells, such as hepatocytes, recruited hepatic macrophages (RHMs), and hepatic stellate cells (HSCs). miR-690 directly inhibits fibrogenesis in HSCs, inflammation in RHMs, and de novo lipogenesis in hepatocytes. When an miR-690 mimic is administered to NASH mice in vivo, all the features of the NASH phenotype are robustly inhibited. During the development of NASH, KCs become miR-690 deficient, and miR-690 levels are markedly lower in mouse and human NASH livers than in controls. KC-specific KO of miR-690 promotes NASH pathogenesis. A primary target of miR-690 is NADK mRNA, and NADK levels are inversely proportional to the cellular miR-690 content. These studies show that KCs play a central role in the etiology of NASH and raise the possibility that miR-690 could emerge as a therapeutic for this condition.
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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.