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Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...
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TGF-β1 Directs TFAM-Mediated Mitochondrial Reprogramming in Oral Submucous Fibrosis.

K M Desai1,2, N A Tadkalkar3, M Amin1

  • 1Oral Biology, Surgery, and Biomedical Engineering, University at Buffalo, Buffalo, NY, USA.

Journal of Dental Research
|December 9, 2025
PubMed
Summary
This summary is machine-generated.

Transforming growth factor-beta (TGF-β) rescues oral fibroblasts from arecoline-induced cell death by modulating mitochondrial function, promoting survival and a fibrotic phenotype. Targeting mitochondria may offer a novel therapeutic strategy for oral submucous fibrosis (OSMF).

Keywords:
TGF-βareca nutarecolinemitochondriamyofibroblastoral submucous fibrosis

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Area of Science:

  • Cell Biology
  • Mitochondrial Bioenergetics
  • Fibrosis Research

Background:

  • Oral submucous fibrosis (OSMF) involves persistent, overactive fibroblasts with altered metabolism and cytoskeletal changes.
  • Arecoline and transforming growth factor-beta (TGF-β) are key mediators implicated in OSMF pathogenesis.
  • Understanding fibroblast behavior and mitochondrial dynamics is crucial for developing effective OSMF treatments.

Purpose of the Study:

  • To evaluate the effects of arecoline and TGF-β on mitochondrial bioenergetics and the phenotype of oral fibroblasts.
  • To investigate the role of mitochondrial fission and fusion in arecoline- and TGF-β-induced fibroblast responses.
  • To correlate in vitro findings with clinical observations in human OSMF tissue samples.

Main Methods:

  • Human oral fibroblasts were treated with arecoline, TGF-β1, and combinations.
  • Cell survival, mitochondrial fusion/fission (OPA-1, MFN-2, DRP-1), and metabolic profiles (TFAM, hexokinase II) were assessed.
  • Real-time PCR, immunofluorescence, Seahorse analysis, and analysis of archival OSMF patient biopsies were employed.

Main Results:

  • Arecoline induced significant oral fibroblast cell death, which was rescued by TGF-β1.
  • Arecoline promoted mitochondrial fission and a glycolytic metabolic profile, while TGF-β1 induced mitochondrial fusion.
  • Combined treatments improved cell survival and mitochondrial bioenergetics, correlating with increased TFAM and vimentin-actin (VA) expression, indicative of a profibrotic phenotype.

Conclusions:

  • TGF-β1 modulates mitochondrial responses to arecoline-induced cytotoxicity, promoting fibroblast survival and a profibrotic phenotype.
  • Increased TFAM and VA-positive fibroblasts in advanced OSMF clinical samples corroborate in vitro findings.
  • Targeting mitochondria in surviving myofibroblasts presents a potential novel therapeutic strategy for OSMF.