ArticleMolecular therapy : the journal of the American Society of Gene Therapy2018
TGF-β Mediates Renal Fibrosis via the Smad3-Erbb4-IR Long Noncoding RNA Axis.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.
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Who cites it
82 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.
- TGF-β/Smad Signaling Pathway in Tubulointerstitial Fibrosis.Frontiers in pharmacology · 2022Pooled it
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Annexin A13 Protects Against Acute Kidney Injury by Inactivating TGF-β/Smad3 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- LncRNA P4HA2-AS1 drives renal interstitial fibrosis via trim32-mediated k63 ubiquitination of ULK1 and autophagic dysregulation.Communications biology · 2026Article
- Lathyrol Exerts Anti-Pulmonary Fibrosis Effects by Activating PPARγ to Inhibit the TGF-β/Smad Pathway.International journal of molecular sciences · 2025Article
- Review
- Role of LncRNA in Pathogenesis, Diagnosis and Treatment of Chronic Kidney Disease.Cell biochemistry and biophysics · 2025Review
- P16-positive senescent cells promote DKD by the dysregulation of glycolysis and mitochondrial metabolism.Cell death discovery · 2025Article
- Zhilong Huoxue Tongyu capsule inhibits hypertensive myocardial fibrosis via balancing TGF-β1/Smad3/Erbb4-IR/miR-29b pathway.Scientific reports · 2025Article
- LncPrep + 96kb inhibits ovarian fibrosis by upregulating prolyl oligopeptidase expression.Molecular medicine reports · 2025Article
- The role of lncRNAs in AKI and CKD: Molecular mechanisms, biomarkers, and potential therapeutic targets.Genes & diseases · 2025Review
- C-reactive protein promotes diabetic kidney disease via Smad3-mediated NLRP3 inflammasome activation.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Traditional Chinese Medicine targeting the TGF-β/Smad signaling pathway as a potential therapeutic strategy for renal fibrosis.Frontiers in pharmacology · 2025Review
- Smad3 Mediates Renal Fibrosis via GPX4-Dependent Ferroptosis.International journal of biological sciences · 2025Article
- Pseudogene GSTM3P1 derived long non-coding RNA promotes ischemic acute kidney injury by target directed microRNA degradation of kidney-protective mir-668.Kidney international · 2024Article
- Genetic variants affecting mitochondrial function provide further insights for kidney disease.BMC genomics · 2024Article
- Mechanisms of norcantharidin against renal tubulointerstitial fibrosis.Pharmacological reports : PR · 2024Review
- Therapeutic potential for renal fibrosis by targeting Smad3-dependent noncoding RNAs.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- Hematopoietic Transcription Factor RUNX1 is Essential for Promoting Macrophage-Myofibroblast Transition in Non-Small-Cell Lung Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Treatment for type 2 diabetes and diabetic nephropathy by targeting Smad3 signaling.International journal of biological sciences · 2024Article
22 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor β (TGF-β)/Smad3 signaling plays a role in tissue fibrosis. We report here that Erbb4-IR is a novel long non-coding RNA (lncRNA) responsible for TGF-β/Smad3-mediated renal fibrosis and is a specific therapeutic target for chronic kidney disease. Erbb4-IR was induced by TGF-β1 via a Smad3-dependent mechanism and was highly upregulated in the fibrotic kidney of mouse unilateral ureteral obstructive nephropathy (UUO). Silencing Erbb4-IR blocked TGF-β1-induced collagen I and alpha-smooth muscle actin (α-SMA) expressions in vitro and effectively attenuated renal fibrosis in the UUO kidney by blocking TGF-β/Smad3 signaling. Mechanistic studies revealed that Smad7, a downstream negative regulator of TGF-β/Smad signaling, is a target gene of Erbb4-IR because a binding site of Erbb4-IR was found on the 3' UTR of Smad7 gene. Mutation of this binding site prevented the suppressive effect of Erbb4-IR on the Smad7 reporter activity; in contrast, overexpression of Erbb4-IR largely inhibited Smad7 but increased collagen I and α-SMA transcriptions. Thus, kidney-specific silencing of Erbb4-IR upregulated renal Smad7 and thus blocked TGF-β/Smad3-mediated renal fibrosis in vivo and in vitro. In conclusion, the present study identified that Erbb4-IR is a novel lncRNA responsible for TGF-β/Smad3-mediated renal fibrosis by downregulating Smad7. Targeting Erbb4-IR may represent a precise therapeutic strategy for progressive renal fibrosis.
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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.