growth factor beta 1 (MedChemExpress)
96
Structured Review
MedChemExpress
growth factor beta 1
Growth Factor Beta 1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 65 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sri+011381/SRI-011381/pm42399357-8-14-18
Average 96 stars, based on 65 article reviews
Growth Factor Beta 1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 65 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/sri+011381/SRI-011381/pm42399357-8-14-18
Average 96 stars, based on 65 article reviews
growth factor beta 1 - by Bioz Stars,
2026-10
96/100 stars
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Modification:Article Title: Macrophage erythropoietin receptor signaling drives macrophage-myofibroblast transition via JAK2/STAT3 and TGF-β1/Smad3 pathways to exacerbate pulmonary fibrosis in mice. Article Snippet: The macrophage-myofibroblast transition (MMT) plays a significant role in the pathogenesis of pulmonary fibrosis; however, the regulatory mechanisms underlying this process are not fully elucidated.. In this study, we provide evidence that signaling through the erythropoietin receptor (EPOR) in macrophages promotes MMT and exacerbates fibrotic progression.. Through an integrated analysis of single-cell data from human idiopathic pulmonary fibrosis (IPF) samples (GSE136831), we identified the presence of MMT characterized by increased EPOR expression in macrophages. H&E Stain:Article Title: Macrophage erythropoietin receptor signaling drives macrophage-myofibroblast transition via JAK2/STAT3 and TGF-β1/Smad3 pathways to exacerbate pulmonary fibrosis in mice. Article Snippet: The macrophage-myofibroblast transition (MMT) plays a significant role in the pathogenesis of pulmonary fibrosis; however, the regulatory mechanisms underlying this process are not fully elucidated.. In this study, we provide evidence that signaling through the erythropoietin receptor (EPOR) in macrophages promotes MMT and exacerbates fibrotic progression.. Through an integrated analysis of single-cell data from human idiopathic pulmonary fibrosis (IPF) samples (GSE136831), we identified the presence of MMT characterized by increased EPOR expression in macrophages. Staining:Article Title: Macrophage erythropoietin receptor signaling drives macrophage-myofibroblast transition via JAK2/STAT3 and TGF-β1/Smad3 pathways to exacerbate pulmonary fibrosis in mice. Article Snippet: The macrophage-myofibroblast transition (MMT) plays a significant role in the pathogenesis of pulmonary fibrosis; however, the regulatory mechanisms underlying this process are not fully elucidated.. In this study, we provide evidence that signaling through the erythropoietin receptor (EPOR) in macrophages promotes MMT and exacerbates fibrotic progression.. Through an integrated analysis of single-cell data from human idiopathic pulmonary fibrosis (IPF) samples (GSE136831), we identified the presence of MMT characterized by increased EPOR expression in macrophages. SYBR Green Assay:Article Title: Macrophage erythropoietin receptor signaling drives macrophage-myofibroblast transition via JAK2/STAT3 and TGF-β1/Smad3 pathways to exacerbate pulmonary fibrosis in mice. Article Snippet: The macrophage-myofibroblast transition (MMT) plays a significant role in the pathogenesis of pulmonary fibrosis; however, the regulatory mechanisms underlying this process are not fully elucidated.. In this study, we provide evidence that signaling through the erythropoietin receptor (EPOR) in macrophages promotes MMT and exacerbates fibrotic progression.. Through an integrated analysis of single-cell data from human idiopathic pulmonary fibrosis (IPF) samples (GSE136831), we identified the presence of MMT characterized by increased EPOR expression in macrophages. Real-time Polymerase Chain Reaction:Article Title: Macrophage erythropoietin receptor signaling drives macrophage-myofibroblast transition via JAK2/STAT3 and TGF-β1/Smad3 pathways to exacerbate pulmonary fibrosis in mice. Article Snippet: The macrophage-myofibroblast transition (MMT) plays a significant role in the pathogenesis of pulmonary fibrosis; however, the regulatory mechanisms underlying this process are not fully elucidated.. In this study, we provide evidence that signaling through the erythropoietin receptor (EPOR) in macrophages promotes MMT and exacerbates fibrotic progression.. Through an integrated analysis of single-cell data from human idiopathic pulmonary fibrosis (IPF) samples (GSE136831), we identified the presence of MMT characterized by increased EPOR expression in macrophages. Saline:Article Title: Microencapsulated 3D culture of human umbilical cord-derived mesenchymal stem cells enhances their therapeutic effect on intrauterine adhesion Article Snippet: .. To further explore the effects of 3D-hUCMSCs on the TGFβ1/Smad signaling pathway, we intervened with the Injection:Article Title: Microencapsulated 3D culture of human umbilical cord-derived mesenchymal stem cells enhances their therapeutic effect on intrauterine adhesion Article Snippet: .. To further explore the effects of 3D-hUCMSCs on the TGFβ1/Smad signaling pathway, we intervened with the Article Title: Fibrotic scar formation after cerebral ischemic stroke: Targeting the Sonic hedgehog signaling pathway for scar reduction Article Snippet: In in vivo experiments, Shh-overexpressing adenovirus (rAd-Shh) (5 μL, 1 × 10 10 pfu/mL, Jima Gene, Suzhou, China) or adenovirus control vector (rAd-HK) (5 μL, 1 × 10 10 pfu/mL, Jima Gene) were injected intracerebroventricularly at 14 days before MCAO/R. .. Control:Article Title: Hyaluronic Acid-Modified N,N,N-trimethyl Chitosan-Poly (β-Aamino Ester) Nanocarriers Loaded with miR210 for Targeted Inhibition of Renal Fibrosis. Article Snippet: BACKGROUND The clinical application of miR210, which possesses the capability to effectively alleviate renal interstitial fibrosis (RIF), is greatly constrained by its poor stability and lack of targeting abilities.. METHODS A hyaluronic acid-modified N,N,N-trimethyl chitosan-poly (b-amino ester) nanoparticle encapsulating miR210 (HTP@miR210) was constructed.. The serum stability, microscopic morphology, particle size, and zeta potential were characterized through gel electrophoresis, transmission electron microscopy, and dynamic light scattering. Incubation:Article Title: Hyaluronic Acid-Modified N,N,N-trimethyl Chitosan-Poly (β-Aamino Ester) Nanocarriers Loaded with miR210 for Targeted Inhibition of Renal Fibrosis. Article Snippet: BACKGROUND The clinical application of miR210, which possesses the capability to effectively alleviate renal interstitial fibrosis (RIF), is greatly constrained by its poor stability and lack of targeting abilities.. METHODS A hyaluronic acid-modified N,N,N-trimethyl chitosan-poly (b-amino ester) nanoparticle encapsulating miR210 (HTP@miR210) was constructed.. The serum stability, microscopic morphology, particle size, and zeta potential were characterized through gel electrophoresis, transmission electron microscopy, and dynamic light scattering. Article Title: Silencing THBS1 in M2 Macrophages Exerts an Inhibitory Effect on Tongue Squamous Cell Carcinoma by Suppressing TGF-β Pathway. Article Snippet: Tongue squamous cell carcinoma (TSCC) is a common oral and maxillofacial malignancy.. Thrombospondin-1 (THBS1), acting in the extracellular matrix, impacts cell migration and proliferation, significantly contributing to tumor development.. We aim to investigate the role of THBS1 in TSCC. |