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Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
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Central Role of Transforming Growth Factor Type Beta 1 in Skeletal Muscle Dysfunctions: An Update on Therapeutic

Johanna Abrigo1,2, Felipe Simon2,3, Daniel Cabrera4,5

  • 1Laboratory of Muscle Pathology, Fragility and Aging, Departamento de Ciencias Biologicas, Facultad de Ciencias Biologicas & Facultad de Medicina, Universidad Andres Bello, Santiago, Chile.

Current Protein & Peptide Science
|November 19, 2017
PubMed

Insights

Transforming Growth Factor Beta 1 (TGF-β1) inhibits muscle regeneration and promotes fibrosis and atrophy. This review explores TGF-β1

Area of Science:

  • Muscle physiology and pathology
  • Cellular biology
  • Regenerative medicine

Background:

  • Transforming Growth Factor Beta 1 (TGF-β1) is a key regulator of skeletal muscle function.
  • TGF-β1 plays a critical role in inhibiting myogenesis and regeneration.
  • It is implicated in muscle pathologies characterized by fibrosis and atrophy.

Purpose of the Study:

  • To review the mechanisms and cellular targets of TGF-β1 in skeletal muscle.
  • To discuss the role of TGF-β1 in muscle regeneration inhibition, fibrosis, and atrophy.
  • To provide an update on therapeutic strategies targeting TGF-β1's detrimental effects.

Main Methods:

  • Literature review of recent scientific publications.
  • Analysis of cellular and molecular mechanisms.
  • Synthesis of current therapeutic approaches.

Main Results:

  • TGF-β1 signaling negatively impacts satellite cell activity and function.
  • The factor is a central mediator in the development of muscle fibrosis and atrophy.
  • Understanding these mechanisms is crucial for developing targeted therapies.

Conclusions:

  • TGF-β1 is a significant detrimental factor in skeletal muscle pathologies.
  • Inhibiting TGF-β1's deleterious actions holds therapeutic potential for muscle diseases.
  • Further research into TGF-β1 inhibition strategies is warranted.
Keywords:
Muscle atrophyblocking antibodiesdystrophyfibrosisrenin angiotensin systemtherapy.

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