Transforming growth factor, beta 1
Transforming growth factor beta 1 (TGF-β1) is a secreted multifunctional cytokine encoded by the TGFB1 gene.
Transforming growth factor beta 1 (TGF-β1) is a secreted multifunctional cytokine encoded by the TGFB1 gene. It belongs to the transforming growth factor beta superfamily and regulates cell proliferation, differentiation, migration, extracellular-matrix production, apoptosis, and immune responses. Transforming growth factor, beta 1 is synthesized as a precursor that is processed and secreted in a latent form; activation releases the mature cytokine, allowing it to bind TGF-β receptors on neighboring or distant cells.
Transforming growth factor, beta 1 Signaling commonly proceeds through receptor-mediated phosphorylation of SMAD2 and SMAD3, which associate with SMAD4 and regulate gene transcription. The pathway is important in tissue repair and immune tolerance, but persistent or excessive Signaling can promote fibrosis, epithelial–mesenchymal transition, and tumor-associated remodeling. In fibrotic disease, Transforming growth factor, beta 1 can activate fibroblasts and pancreatic stellate cells, increase extracellular-matrix deposition, and interact with inflammatory mediators such as Interleukin-1β (IL-1β), Interleukin-6 (IL-6), and Tumor necrosis factor-α (TNF-α)-α. In immunity, Transforming growth factor, beta 1 produced by cells including Macrophages can support regulatory T cell differentiation and influence the balance between regulatory T cells and Th17 cells. These properties make Transforming growth factor, beta 1 a major biological target in fibrosis, Cancer biology, inflammatory disease, cardiovascular research, and immune-modulating therapies.
Rebuilt from PubMed 18 Sept 2026 · no new papers today
Where the papers sit
9 papers study transforming growth factor, beta 1 directly. The themes below are drawn from those 9. 1 paradigm shift follows.
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Inflammatory Organ Injury : Anti-inflammatory interventions are being linked to TGFβ, IL-6/IL-1β and MAPK/AP-1 signaling across pancreatic, cardiac, renal and metabolic injury. The work remains preclinical and mechanism-focused, with network analyses guiding candidate pathways rather than establishing a common therapy. 4 papers · 44.4%
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Fibroblast Activation and Fibrosis : TGFβ1/Smad-driven fibroblast activation is increasingly framed as intercellular crosstalk, with exosomal LINC01605 and macrophage IL4R/JAK/STAT signaling as intervention points. TGFβ isoform differences also recur in meningioma. 3 papers · 33.3%
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Collagen-Based Tissue Repair : Collagen-based nanomaterials are being developed to restore skin or dentin barriers while supporting TGFβ1 release, stem-cell attachment and differentiation. Recurring endpoints are hydration, collagen remodeling and matrix repair, but evidence remains largely in vitro. 2 papers · 22.2%
TGF-β1 can support repair and immune protection rather than functioning only as a profibrotic signal
In the rat myocardial ischemia–reperfusion model treated with the adiponectin-receptor agonist peptide ALY688, and in dentin-derived dental stem cells exposed to chitosan nanoparticles, TGF-β1 produced beneficial effects rather than the fibroblast-activating and fibrotic effects emphasized elsewhere in the set. ALY688-induced macrophage secretion of TGF-β1 promoted regulatory T-cell differentiation and suppressed inflammatory signaling, improving cardiac remodeling, while chitosan nanoparticle–mediated TGF-β1 release enhanced stem-cell mineralization and odontogenic/osteogenic differentiation 42521105Jul 42150727May. Together, these independent models replace a uniformly profibrotic interpretation with a context-dependent one in which TGF-β1 can be therapeutically recruited for immune regulation and tissue regeneration.
Recent Findings on Transforming growth factor, beta 1
Inflammatory Cytokine Signaling: CUR-IPA, baicalin, HLJDD, and ALY688 place TGFβ1 within inflammatory and tissue-remodeling pathways across metabolic, cardiac, pancreatic, and renal models. CUR-IPA identified TGFβ1 as a central hub in diabetes-associated cognitive decline and showed stable molecular docking and simulation-based binding 42521900Jul. ALY688 instead used macrophage-derived TGFβ1 to promote regulatory T cell differentiation, suppress inflammasome and IL-1β/IL-23/IL-6 signaling, and protect the intestinal barrier 42521105Jul. Baicalin and HLJDD reduced inflammation and fibrosis through TGF-β1/SMAD3 or AGEs-RAGE/MAPK/AP-1 signaling, respectively 42397030Jul42035996Apr. These results differ in TGFβ1’s immediate role: ALY688 uses macrophage TGFβ1 in an anti-inflammatory circuit, whereas baicalin and HLJDD suppress TGFβ1-linked profibrotic signaling.
Fibroblast TGF-β Signaling: Dupilumab, keratinocyte-derived exosomes, and meningioma tissue profiles connect TGF-β1 signaling to fibroblast activation, intercellular communication, and disease heterogeneity. Dupilumab suppressed TGF-β1-induced fibroblast activation and disrupted profibrotic macrophage-fibroblast crosstalk by inhibiting TGF-β1/Smad and IL4R/JAK/STAT pathways in preclinical pulmonary fibrosis models 42747578Sep. TGF-β1-stimulated keratinocytes released exosomes containing LINC01605, which sponged miR-370-3p, increased TGFBR2 expression, and amplified TGF-β1/Smads signaling in human dermal fibroblasts 42320250Jun. Meningioma samples showed a contrasting grade-dependent pattern, with reduced TGF-β1 and increased TGF-β2 and TGF-β3 in grade 2 tumors 42608612Aug. This divergence supports tissue-specific TGF-β profiling alongside therapies that interrupt macrophage-fibroblast or exosome-mediated communication.
Collagen-Based Tissue Repair: Collagen and chitosan materials use TGF-β1-related matrix remodeling to improve epithelial or dentin-associated tissue repair. Supra-Coll-Nano activated TGF-β1/Smad3, increased collagens and barrier proteins including Filaggrin and Loricrin, and improved stratum corneum hydration, elasticity, and crow’s feet wrinkles in clinical evaluations 42480655Jul. Chitosan nanoparticles promoted TGF-β1 release from dentin and supported Dental Stem Cells SV40 attachment, calcium deposition, and osteogenic/odontogenic differentiation in vitro 42150727May. The materials differ in application and evidence stage, with Supra-Coll-Nano targeting transdermal skin repair and chitosan nanoparticles targeting dentin conditioning and stem-cell responses. Both studies support material designs that regulate TGF-β1 release or signaling while organizing collagen-associated repair.
Written from 9 PubMed abstracts, each one cited by PMID above. Published: 2026-08-20. Last written: 2026-09-18 by GPT. Drafted by language models from published abstracts; not medical advice.