ArticleBioactive materials2024
Engineered SPIONs functionalized with endothelin a receptor antagonist ameliorate liver fibrosis by inhibiting hepatic stellate cell activation.
Article in Bioactive materials, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Liver fibrosis: Pathogenesis and innovative nanoparticle-based therapeutic strategies.International journal of pharmaceutics: X · 2026Review
- The Liver-Heart Axis in Rheumatoid Arthritis: Associations of Liver Fibrosis, Organokines, Endothelin-1, and Cardiovascular Risk.International journal of molecular sciences · 2026Article
- NUP85 Mediates Endoplasmic Reticulum Stress through the USP47/ASK1 Signaling Pathway to Regulate the Progression of Liver Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Recent Updates on Molecular and Physical Therapies for Organ Fibrosis.Molecules (Basel, Switzerland) · 2025Review
- The Involvement of Endothelin-1 in Sepsis and Organ Dysfunction-A Novel Biomarker in Patient Assessment.Biomedicines · 2025Review
- The Role of Endothelin-1, Kidney Function and Diabetes in Patients With Coronary Artery Disease Underwent Percutaneous Coronary Intervention.Journal of diabetes · 2025Article
- Liraglutide inhibits the proliferation of rat hepatic stellate cells under high glucose conditions by suppressing the ERK signaling pathway.Scientific reports · 2025Article
- Exploring hepatic stellate cell-driven fibrosis: therapeutic advances and future perspectives.ADMET & DMPK · 2025Review
- Advances in intrahepatic and extrahepatic vascular dysregulations in cirrhotic portal hypertension.Frontiers in medicine · 2025Review
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Authors and funding
9 authors.
Funding
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Abstract
Endothelin-1/endothelin A receptor (ET-1/ETAR) pathway plays an important role in the progression of liver fibrosis by activating hepatic stellate cells (HSCs) - a key cell type involved in the pathogenesis of liver fibrosis. Inactivating HSCs by blocking the ET-1/ETAR pathway using a selective ETAR antagonist (ERA) represents a promising therapeutic approach for liver fibrosis. Unfortunately, small-molecule ERAs possess limited clinical potential due to poor bioavailability, short half-life, and rapid renal clearance. To improve the clinical applicability, we conjugated ERA to superparamagnetic iron-oxide nanoparticles (SPIONs) and investigated the therapeutic efficacy of ERA and ERA-SPIONs in vitro and in vivo and analyzed liver uptake by in vivo and ex vivo magnetic resonance imaging (MRI), HSCs-specific localization, and ET-1/ETAR-pathway antagonism in vivo. In murine and human liver fibrosis/cirrhosis, we observed overexpression of ET-1 and ETAR that correlated with HSC activation, and HSC-specific localization of ETAR. ERA and successfully synthesized ERA-SPIONs demonstrated significant attenuation in TGFβ-induced HSC activation, ECM production, migration, and contractility. In an acute CCl
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