ArticleLaboratory investigation; a journal of technical methods and pathology2017
Paired related homeobox protein 1 regulates PDGF-induced chemotaxis of hepatic stellate cells in liver fibrosis.
Article in Laboratory investigation; a journal of technical methods and pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- From mechanisms to anti-fibrotic drugs in hepatic stellate cell research: a global bibliometric analysis with patent and clinical perspectives (2000-2025).Frontiers in pharmacology · 2025Pooled it
- Prrx1 promotes mesangial cell proliferation and kidney fibrosis through YAP in diabetic nephropathy.Journal of pharmaceutical analysis · 2025Article
- Neuronal injury and hepatotoxicity: astrocytes and stellate cells convergence and their role in tissue repair.Frontiers in neuroscience · 2025Review
- Article
- The roles of ETS transcription factors in liver fibrosis.Human cell · 2023Review
- A novel tumor-homing TRAIL variant eradicates tumor xenografts of refractory colorectal cancer cells in combination with tumor cell-targeted photodynamic therapy.Drug delivery · 2022Article
- The Effects of Irisin on the Interaction between Hepatic Stellate Cell and Macrophage in Liver Fibrosis.Endocrinology and metabolism (Seoul, Korea) · 2022Article
- Time and phenotype-dependent transcriptome analysis in AAV-TGFβ1 and Bleomycin-induced lung fibrosis models.Scientific reports · 2022Article
- Epithelial-mesenchymal transition and its transcription factors.Bioscience reports · 2022Review
- Metabolic Reprogramming of Liver Fibrosis.Cells · 2021Review
- Single-cell and bulk transcriptomics of the liver reveals potential targets of NASH with fibrosis.Scientific reports · 2021Article
- COL6A3 expression in adipose tissue cells is associated with levels of the homeobox transcription factor PRRX1.Scientific reports · 2020Article
- Cytochrome P4501B1 in bone marrow is co-expressed with key markers of mesenchymal stem cells. BMS2 cell line models PAH disruption of bone marrow niche development functions.Toxicology and applied pharmacology · 2020Article
- Expression of hepatic stellate cell activation-related genes in HBV-, HCV-, and nonalcoholic fatty liver disease-associated fibrosis.PloS one · 2020Article
- Insulin receptor substrate 2 (IRS2) deficiency delays liver fibrosis associated with cholestatic injury.Disease models & mechanisms · 2019Article
- Transcriptional regulation of Hepatic Stellate Cell activation in NASH.Scientific reports · 2019Article
- Transcriptome analysis reveals differentially expressed genes between human primary bone marrow mesenchymal stem cells and human primary dermal fibroblasts.Turkish journal of biology = Turk biyoloji dergisi · 2019Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of the platelet-derived growth factor (PDGF)/PDGF beta receptor (PDGFβR) axis has a critical role in liver fibrosis. However, the mechanisms that regulate the PDGF signaling are yet to be elucidated. The present study demonstrates that paired related homeobox protein 1 (Prrx1) is involved in PDGF-dependent hepatic stellate cell (HSCs) migration via modulation of the expression of metalloproteinases MMP2 and MMP9. PDGF elevated the level of Prrx1 through the activation of ERK/Sp1 and PI3K/Akt/Ets1 pathways. In vivo, an adenoviral-mediated Prrx1 shRNA administration attenuated liver fibrosis in thioacetamide-induced fibrotic models. These studies reveal a role of Prrx1 as a modulator of PDGF-dependent signaling in HSCs, and inhibiting its expression may offer a therapeutic approach for hepatic 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.