TGFB1

TGFB1

Overview

TGFB1 encodes transforming growth factor beta-1 (TGF-β1), a secreted cytokine and multifunctional signaling molecule in the transforming growth factor beta family. It is a central regulator of cell growth, differentiation, extracellular matrix production, immune modulation, wound repair, and tissue remodeling. Through canonical Smad2/3 signaling and related non-canonical pathways, TGF-β1 can promote either homeostatic repair or pathological fibrosis depending on cellular context, dose, and disease state.

In biomedical research, TGFB1 is frequently studied as both a mechanistic driver and a therapeutic target. It is especially relevant in fibrosis, cancer progression, immune suppression, cartilage regeneration, diabetic wound healing, and transplant biology. In tumors, TGFB1 is often associated with immunosuppressive microenvironments and poor prognosis; in regenerative settings, it can support matrix deposition and lineage-specific differentiation, including chondrogenesis and wound repair.

Recent Publications Focus

Below is a summary of the newest research publications targeting TGFB1 (sorted by publication date).

  • 2026-08-15 — Hepatocellular carcinoma and immune suppression

    • An integrative multi-omics study identified UBE2C as a central hub gene and prognostic biomarker in hepatocellular carcinoma. Spatial transcriptomics showed that UBE2C-high regions were associated with proliferative niches displaying immunosuppressive features, including TGFB1 enrichment, impaired CXCL9-CXCR3 signaling, and exclusion of cytotoxic T cells.
    • These findings place TGFB1 within a tumor microenvironment associated with immune evasion and poorer response to immunotherapy, reinforcing its role as a marker of suppressive stromal or immune-active signaling in cancer.
  • 2026-06-01 — Diabetic nephropathy and Astragalus membranaceus

    • A systematic pharmacological evaluation and mechanistic study of fermented Astragalus membranaceus broth (FA) in diabetic nephropathy reported that chemical profiling identified 14 bioactive components.
    • Network pharmacology highlighted TGFB1 among the core targets, together with STAT3 and IL6, and implicated pathways including AGE-RAGE, HIF-1, and FoxO. This suggests TGFB1 may participate in the therapeutic network underlying the renoprotective effects of fermented Astragalus preparations.
  • 2026-05-28 — Chondrogenic differentiation in spheroids, HAMA hydrogels, and bioprinted constructs

    • Human periosteum-derived cells were compared across spheroids, HAMA hydrogels, and bioprinted constructs in the presence of kartogenin or TGF-β1.
    • The study found that when combined with TGF-β1, HAMA-encapsulated spheroids showed enhanced chondrogenesis, including stronger collagen fiber organization, increased glycosaminoglycan deposition, and positive Safranin O staining, which was absent in material-free conditions. This supports TGFB1 as a potent driver of cartilage-like matrix formation in engineered tissue systems.
  • 2026-05-18 — Cardiac fibrosis in diabetic cardiomyopathy

    • In a rat model of diabetic cardiomyopathy, oleuropein was reported to attenuate cardiac fibrosis through modulation of the TGF-β1/Smad pathway.
    • The publication states that TGF-β1, via Smad2/3 signaling, promotes fibrotic gene expression. This reinforces TGFB1 as a key pro-fibrotic mediator in diabetic cardiac remodeling and a pathway node responsive to anti-fibrotic intervention.
  • 2026-05-16 — Pancreatic cancer prognosis and ferroptosis-related analysis

    • An integrative multi-omics analysis identified a core ferroptosis signature and validated resveratrol as a novel inducer in pancreatic cancer.
    • Clinical validation showed high CTSB/TFRC protein expression in pancreatic ductal adenocarcinoma, and high TGFB1 predicted poor prognosis. In this context, TGFB1 appears to be associated with adverse clinical outcome and may reflect a tumor-promoting or immunosuppressive state.
  • 2026-05-15 — Diabetic wound healing with functional hyaluronic acid/gelatin hydrogel

    • A functional hyaluronic acid/gelatin hydrogel was shown to accelerate closure and healing of diabetic wounds.
    • The treatment was associated with upregulation of pro-healing markers including TGF-β1, α-SMA, and p-Smad2, indicating activation of a repair-associated signaling axis. These findings support TGFB1 as part of the molecular response linked to improved wound repair.
  • 2026-05-14 — Decellularized dermal scaffold and biophysical stimulation in type 2 diabetic wounds

    • In a type 2 diabetic wound model, a decellularized dermal scaffold combined with adjunct biophysical stimulation improved angiogenic, inflammatory, and matrix remodeling responses.
    • Treated wounds showed elevated levels of pro-regenerative mediators, including transforming growth factor-β1 (TGF-β1) and VEGF, with maximal expression in the combined treatment group. This indicates TGFB1 participates in the regenerative microenvironment promoted by scaffold-based and biophysical interventions.
  • 2026-05-10 — extracellular vesicle engineering for dendritic cell vaccines

    • Researchers engineered extracellular vesicles from colon carcinoma MC38 cells by lentiviral modification to overexpress IL-18 and/or use small hairpin RNA targeting TGF-β1 or IL-10, aiming to enhance the immunogenic potential of tumor-derived vesicles for next-generation dendritic cell vaccines.
    • This study positions TGFB1 as an immunosuppressive factor whose reduction may improve antigenic or vaccine-related immune activation.
  • 2026-05-01 — Kidney transplant rejection and urinary exosomal microRNAs

    • In 70 kidney transplant recipients, urinary exosomal microRNAs were investigated as biomarkers associated with subclinical acute T-cell-mediated rejection.
    • In vitro exposure of epithelial cells of the proximal tubule to TGF-β1 reduced miR-7975 expression within urinary exosomes, implicating these cells as a potential source of exosomal miR-7975. This links TGFB1 to epithelial signaling changes relevant to transplant monitoring and rejection biology.
  • 2026-05-01 — Osteosarcoma and PTGS2/TGFB1

    • A study on Liquidambaris fructus reported inhibition of osteosarcoma through PTGS2/TGFB1 and regulation of efferocytosis.
    • Although the publication context is brief, it indicates TGFB1 was considered part of a target axis associated with anti-tumor activity and immune-cell clearance processes.
  • 2026-04-28 — Cartilage regeneration with thermosensitive hydrogel and exosomes

    • A functionalized thermosensitive hydrogel was used to regulate the immune microenvironment and stem cell differentiation to enhance cartilage regeneration.
    • Mechanistically, HBC@Sr@CPC-EXOs activated TGF-β1/Smad2/3 while suppressing Notch, driving bone marrow stromal cell (BMSC) chondrogenic differentiation. This supports TGFB1 as a central mediator of pro-chondrogenic signaling in regenerative biomaterials.
  • 2026-05-10 — Tumor extracellular vesicles and immunogenicity

    • In a separate extracellular vesicle engineering study, tumor-derived vesicles were modified by overexpressing IL-18 and/or using shRNA targeting TGF-β1 to improve their immunogenic potential.
    • Together with the dendritic cell vaccine context, this underscores TGFB1 as a target for reducing tumor-associated immunosuppression and enhancing anti-tumor immune responses.

Summary of recurring themes

Across these recent studies, TGFB1 appears repeatedly as:

  • a pro-fibrotic mediator in diabetic cardiomyopathy and other remodeling settings,
  • a pro-regenerative signal in diabetic wound healing and cartilage engineering,
  • an immunoregulatory and often immunosuppressive factor in cancer and transplant-related contexts,
  • and a mechanistic node in biomaterial-assisted tissue repair, extracellular vesicle engineering, and pathway-focused pharmacology.

The publications collectively highlight the context dependence of TGFB1 biology: the same signaling axis can support tissue repair and matrix formation in regenerative settings while also promoting fibrosis, immune exclusion, or poor prognosis in disease.

Method PMIDs

  • [PMID 42067915]

Result PMIDs

  • [PMID 42155390]
  • [PMID 42142137]
  • [PMID 41831972]
  • [PMID 42133132]

Target PMIDs

  • [PMID 42009593]
  • [PMID 42102888]
  • [PMID 42151222]
  • [PMID 41879412]
  • [PMID 41969062]
  • [PMID 41780683]