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Remote limb ischemic conditioning alleviates nonalcoholic steatohepatitis via extracellular vesicle-mediated muscle-liver crosstalk [hEV_RNAseq]

ABSTRACT: Nonalcoholic steatohepatitis (NASH) is an advanced form of nonalcoholic fatty liver disease with adverse outcomes that currently lacks approved medication. Muscle-liver interaction has emerged as one of the critical determinants governing NASH progression. Here, we report that remote limb ischemic conditioning (RIC), a clinically validated therapy for distant ischemic organ protection by transient muscle ischemia, significantly alleviated NASH in different mouse models. The anti-NASH effect of chronic RIC treatment was mediated by the muscle-to-liver transfer of extracellular vesicles (EVs) and their cargo microRNAs, leading to elevation of miR-181d-5p in the liver. Hepatic miR-181d-5p overexpression faithfully mirrored the benefits of RIC treatment via suppression of nuclear receptor 4A3. Furthermore, administration of circulating EVs from human volunteers undergoing RIC treatment improved NASH phenotypes and transcriptomic perturbations in primary human hepatocytes and animal models. Our data underscore the translational potential of RIC treatment for NASH management and extend our understanding of muscle-liver crosstalk.

ORGANISM(S): Mus musculus

PROVIDER: GSE255527 | GEO | 2025/11/25

REPOSITORIES: GEO

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Remote limb ischemic conditioning alleviates nonalcoholic steatohepatitis via extracellular vesicle-mediated muscle-liver crosstalk [miR_181_RNAseq]

Project description:Nonalcoholic steatohepatitis (NASH) is an advanced form of nonalcoholic fatty liver disease with adverse outcomes that currently lacks approved medication. Muscle-liver interaction has emerged as one of the critical determinants governing NASH progression. Here, we report that remote limb ischemic conditioning (RIC), a clinically validated therapy for distant ischemic organ protection by transient muscle ischemia, significantly alleviated NASH in different mouse models. The anti-NASH effect of chronic RIC treatment was mediated by the muscle-to-liver transfer of extracellular vesicles (EVs) and their cargo microRNAs, leading to elevation of miR-181d-5p in the liver. Hepatic miR-181d-5p overexpression faithfully mirrored the benefits of RIC treatment via suppression of nuclear receptor 4A3. Furthermore, administration of circulating EVs from human volunteers undergoing RIC treatment improved NASH phenotypes and transcriptomic perturbations in primary human hepatocytes and animal models. Our data underscore the translational potential of RIC treatment for NASH management and extend our understanding of muscle-liver crosstalk.

2025-11-25 | GSE255526 | GEO

Remote limb ischemic conditioning alleviates nonalcoholic steatohepatitis via extracellular vesicle-mediated muscle-liver crosstalk [EV miRNA]

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Metabolic crosstalk between skeletal muscle cells and liver through IRF4-FSTL1 in 2 nonalcoholic steatohepatitis

Project description:In this study Guo et al. revealed an endocrine pathway regulated by skeletal muscle IRF4 that manipulates liver pathology. Mice with skeletal muscle specific ablation of IRF4 show ameliorated liver steatosis, inflammation, and fibrosis, without changes in body weight on nonalcoholic steatohepatitis (NASH) diet. Proteomics analysis of mouse serum suggested that follistatin-like protein 1 (FSTL1) might link the communication between muscle and liver. Dual luciferase assays showed that IRF4 could transcriptionally regulate FSTL1 and reconstitution of FSTL1 expression in muscle of F4MKO mice was sufficient to restore the liver pathology. Furthermore, co-culture experiments verified that FSTL1 exerts its function in hepatocyte, macrophage, and hepatic satellite cells through CD14 and DIP2A, CD14, DIP2A, respectively. In human, serum FSTL1 is increased in NASH patients, but the mRNA level of Fstl1 and its receptors are decreased in NASH liver biopsy, suggesting the increased serum FSTL1 is from skeletal muscle as studied in F4MKO mice. These data unveiled a signaling pathway from skeletal muscle to liver via IRF4-FSTL1-DIP2A/CD14 in the pathogenesis of NASH.

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Expression data from mouse liver treated with metformin

Project description:Optimal treatment for nonalcoholic steatohepatitis (NASH) has not yet been established, particularly for individuals without diabetes. We examined the effects of metformin, commonly used to treat patients with type 2 diabetes, on liver pathology in a non-diabetic NASH mouse model. Eight-week-old C57BL/6 mice were fed a methionine- and choline-deficient (MCD) + high fat (HF) diet with or without 0.1% metformin for 8 weeks.

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Sonic hedgehog-heat shock protein 90β axis promotes the development of nonalcoholic steatohepatitis (miRNA-Seq)

Project description:The incidence rate of nonalcoholic steatohepatitis (NASH) is on the rise with no effective clinical treatment available to date. Understanding the key molecular mechanism underlying the process of NASH can provide theoretical support for the development of safe and effective therapeutic drugs. Sonic hedgehog (SHH) and heat shock protein 90β (HSP90β) have been implicated in NASH but their molecular mechanisms of action remain elusive. HSP90β was found to be a key SHH downstream molecule that promoted NASH processes In hepatocytes, SHH reduced HSP90β ubiquitylation through deubiquitylase USP31, thus preventing HSP90β degradation and promoting hepatic lipid synthesis. As an important component protein in the formation of exosomes, HSP90β is high in high fructose, high fat, and high cholesterol (HFFC) diet-induced NASH mouse model, leading to secretion of exosomes enriched with miR-28-5p. miR-28-5p directly targets and decreases Rap1b levels, which in turn promote NF-κB transcriptional activity in macrophages and stimulate the expression of inflammatory factors. Genetic deletion, pharmacological inhibition of the SHH-HSP90β axis, or delivery of miR-28-5p to macrophages in the liver, impaired NASH symptomatic development. Importantly, analysis of NASH patient sera revealed a markedly higher abundance of miR-28-5p compared to healthy donors. Taken together, the SHH-HSP90β-miR-28-5p axis offers promising therapeutic targets against NASH, and serum miR-28-5p may serve as a novel NASH diagnostic biomarker.

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Sonic hedgehog-heat shock protein 90β axis promotes the development of nonalcoholic steatohepatitis (RNA-Seq)

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Integrative Omics Reveals Subtle Molecular Perturbations Following Ischemic Conditioning in a Porcine Kidney Transplant Model

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