Clinical Relevance and Mechanisms of Antagonism Between the BMP and Activin/TGF-β Signaling Pathways
Autor: | Aaron M. Hudnall, Jonathan W. Lowery, Jon W. Arthur |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Complementary and Manual Therapy medicine.medical_specialty Cell signaling Bone morphogenetic protein 03 medical and health sciences 0302 clinical medicine Transforming Growth Factor beta Internal medicine medicine Humans Tissue homeostasis Activin type 2 receptors biology business.industry Transforming growth factor beta Cell biology BMPR2 030104 developmental biology Endocrinology Complementary and alternative medicine 030220 oncology & carcinogenesis Bone Morphogenetic Proteins biology.protein Signal transduction business Signal Transduction Transforming growth factor |
Zdroj: | Journal of Osteopathic Medicine. 116:452-461 |
ISSN: | 2702-3648 |
DOI: | 10.7556/jaoa.2016.089 |
Popis: | The transforming growth factor β (TGF-β) superfamily is a large group of signaling molecules that participate in embryogenesis, organogenesis, and tissue homeostasis. These molecules are present in all animal genomes. Dysfunction in the regulation or activity of this superfamily’s components underlies numerous human diseases and developmental defects. There are 2 distinct arms downstream of the TGF-β superfamily ligands—the bone morphogenetic protein (BMP) and activin/TGF-β signaling pathways—and these 2 responses can oppose one another’s effects, most notably in disease states. However, studies have commonly focused on a single arm of the TGF-β superfamily, and the antagonism between these pathways is unknown in most physiologic and pathologic contexts. In this review, the authors summarize the clinically relevant scenarios in which the BMP and activin/TGF-β pathways reportedly oppose one another and identify several molecular mechanisms proposed to mediate this interaction. Particular attention is paid to experimental findings that may be informative to human pathology to highlight potential therapeutic approaches for future investigation. |
Databáze: | OpenAIRE |
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