ArticleNature nanotechnology2021
Hepatic macrophages act as a central hub for relaxin-mediated alleviation of liver fibrosis.
Article in Nature nanotechnology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 131 citations in OpenAlex.
- Magnesium-tannic acid nanomedicines reprogram pro-fibrotic macrophages for hepatic fibrosis treatment via restoring endoplasmic reticulum homeostasis.Journal of nanobiotechnology · 2026Article
- Immune profiling links autoimmune hepatitis to human herpesvirus 6 and relaxin receptor antigens.The Journal of experimental medicine · 2026Article
- Circular RNA encoding relaxin-2 as a potential therapy for liver fibrosis.Molecular therapy. Nucleic acids · 2026Article
- TRIM13 in situ engineering boosts anti-inflammatory capacity of CAR-Ms for liver fibrosis therapy.Nature communications · 2026Article
- Engineered exosomes from umbilical cord mesenchymal stem cells with pPB modification attenuate hepatic fibrosis via hepatic stellate cell targeting.Journal of translational medicine · 2026Article
- Macrophage-Targeted Magnesium Ion-Nourisher for NLRP3 Inflammasome Inhibition to Enhance Liver Inflammatory Disease Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeted Hepatic Delivery of Bioactive Molecules via Nanovesicles: Recent Developments and Emerging Directions.Journal of personalized medicine · 2025Review
- Matrix mechanical remodeled carrier-free nanosystem for programmable closed-loop reversal of liver fibrosis via STING alkylation.Science advances · 2025Article
- Activating PEG host to enable spatially controlled surface functionalization of nanocarriers for biomedical applications.Science advances · 2025Article
- Hydrogel Loaded with Aminoethyl Anisamide-Modified Exosomes Attenuates Hepatic Fibrosis by Targeting Activated Hepatic Stellate Cells.ACS nano · 2025Article
- Genomic medicine in hepatology: mechanisms and liver treatment strategies.Molecular medicine (Cambridge, Mass.) · 2025Review
- Dissecting the mechanisms of MASLD fibrosis in the era of single-cell and spatial omics.The Journal of clinical investigation · 2025Review
- Notoginsenoside R2 attenuates hepatic fibrosis via STAT3-dependent hepatic stellate cells senescence induction and inflammatory microenvironment suppression.Journal of ginseng research · 2025Article
- Artesunate Nanoplatform Targets the Serine-MAPK Axis in Cancer-Associated Fibroblasts to Reverse Photothermal Resistance in Triple-Negative Breast Cancer.Advanced materials (Deerfield Beach, Fla.) · 2025Article
- Extracellular vesicle-based drug overview: research landscape, quality control and nonclinical evaluation strategies.Signal transduction and targeted therapy · 2025Review
- Biomimetic nanoparticles for targeted therapy of liver disease.RSC pharmaceutics · 2025Review
- Advances in nanotechnology for the diagnosis and management of metabolic dysfunction-associated steatotic liver disease.Asian journal of pharmaceutical sciences · 2025Review
- Why do lipid nanoparticles target the liver? Understanding of biodistribution and liver-specific tropism.Molecular therapy. Methods & clinical development · 2025Review
- Current Therapeutic Landscape for Metabolic Dysfunction-Associated Steatohepatitis.International journal of molecular sciences · 2025Review
- A chimeric peptide promotes immune surveillance of senescent cells in injury, fibrosis, tumorigenesis and aging.Nature aging · 2025Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Relaxin is an antifibrotic peptide hormone previously assumed to directly reverse the activation of hepatic stellate cells for liver fibrosis resolution. Using nanoparticle-mediated delivery, here we show that, although relaxin gene therapy reduces liver fibrosis in vivo, in vitro treatment fails to induce quiescence of the activated hepatic stellate cells. We show that hepatic macrophages express the primary relaxin receptor, and that, on relaxin binding, they switch from the profibrogenic to the pro-resolution phenotype. The latter releases exosomes that promote the relaxin-mediated quiescence of activated hepatic stellate cells through miR-30a-5p. Building on these results, we developed lipid nanoparticles that preferentially target activated hepatic stellate cells in the fibrotic liver and encapsulate the relaxin gene and miR-30a-5p mimic. The combinatorial gene therapy achieves synergistic antifibrosis effects in models of mouse liver fibrosis. Collectively, our findings highlight the key role that macrophages play in the relaxin-primed alleviation of liver fibrosis and demonstrate a proof-of-concept approach to devise antifibrotic strategies through the complementary application of nanotechnology and basic science.
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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.