ArticleMolecular therapy. Nucleic acids2023
Angiotensin II mediates hypertensive cardiac fibrosis via an Erbb4-IR-dependent mechanism.
Article in Molecular therapy. Nucleic acids, 2023. 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, 9 citations in OpenAlex.
- Targeting C/EBPβ to Suppress Myocardial Fibrosis in Hypertensive Heart Disease: Role of the ACE2/Ang-(1-7) Pathway.Journal of cellular and molecular medicine · 2026Article
- Annexin A13 Protects Against Acute Kidney Injury by Inactivating TGF-β/Smad3 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Molecular Interplay between hypertension and dyslipidemia in cardiovascular pathogenesis: toward precision-based therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- The Leaf Aqueous and Ethanolic Extracts ofAdvances in pharmacological and pharmaceutical sciences · 2026Article
- Therapeutic Targets for Myocardial Fibrosis: A Comprehensive Review of Current and Emerging Approaches.Cardiovascular & hematological disorders drug targets · 2026Review
- Zhilong Huoxue Tongyu capsule inhibits hypertensive myocardial fibrosis via balancing TGF-β1/Smad3/Erbb4-IR/miR-29b pathway.Scientific reports · 2025Article
- Supplementation with the Postbiotic BPL1™-HT (Heat-InactivatedAntioxidants (Basel, Switzerland) · 2025Article
- Review
- Identification of ligand and receptor interactions in CKD and MASH through the integration of single cell and spatial transcriptomics.PloS one · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor β (TGF-β)/Smad3 plays a vital role in hypertensive cardiac fibrosis. The long non-coding RNA (lncRNA) Erbb4-IR is a novel Smad3-dependent lncRNA that mediates kidney fibrosis. However, the role of Erbb4-IR in hypertensive heart disease remains unexplored and was investigated in the present study by ultrasound-microbubble-mediated silencing of cardiac
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Registered trials
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