Role of molecular signaling pathways in the pathogenesis of adenomyosis

2021 ◽  
Vol 70 (3) ◽  
pp. 121-134
Author(s):  
Maria A. Shalina ◽  
Maria I. Yarmolinskaya ◽  
Elena A. Netreba ◽  
Alexandra K. Beganova

The prevalence of genital endometriosis and adenomyosis, in particular, is tending to increase. The lack of a complete understanding of the pathogenetic mechanisms and multifactorial causes of adenomyosis, the low effectiveness of existing drug therapy, and the importance of preserving reproductive function make it necessary to further study the pathogenesis of the disease, search for new non-invasive highly informative diagnostic methods and develop a new strategy for pathogenically based drug therapy. The review presents current data on the role of signaling pathways in the pathogenesis of the development of adenomyosis based on domestic and foreign literature sources retrieved from the electronic databases PubMed, CyberLeninka, and Google Scholar in the period from 1999 to 2020. Considerable emphasis is placed on the discussion of the research results in recent years. Based on the analysis, the role of transforming growth factor (TGF), vascular endothelial growth factor (VEGF), dual-specificity protein phosphatase (PTEN), Notch receptors, and eukaryotic translation initiation factors (eIFs) in the signaling of adenomyosis is presented. Further advanced study of signaling pathways in the pathogenesis of adenomyosis will allow developing highly specific and highly sensitive markers for non-invasive diagnostics, as well as new directions for drug treatment of the disease.

Author(s):  
S. V. Grigoryan ◽  
L. G. Azarapetyan ◽  
K. G. Adamyan

Atrial fibrillation is the most prevalent arrhythmia, and tends to progress. Any structural changes in the heart may lead to its progressive remodelling with increased deposition of connective tissue and fibrosis. Predominance of collagen types I and III synthesis over its degradation leads to accumulation of fibers and to fibrosis. Increase of atrial fibrosis is usually found on autopsy and biopsy. There is relation revealed, of atrial fibrosis grade and postsurgery atrial fibrillation. The mechanisms participating in the structural remodelling and progression of atrial fibrosis are not studied well enough, but there is known role of renin-angiotensinaldosterone system, transforming growth factor, inflammation and matrix metalloproteases. As an alternative, one should consider non-invasive diagnostic methods: magnetic resonance imaging of the heart and biomarkers level measurement. Hyperactivation of the renin-angiotensin-aldosterone system facilitates structural remodelling of the heart and progression of atrial fibrosis. Hyperexpression of the transforming growth factor leads to selective atrial fibrosis, heterogeneity of excitation conduction and fibrillation onset. Matrix metalloproteases are the marker of extracellular degradation. Study of fibrosis biomarkers makes it to increase significantly the efficacy of atrial fibrillation course prediction.


2011 ◽  
Vol 31 (2) ◽  
pp. E7 ◽  
Author(s):  
Harvey Chim ◽  
Sunil Manjila ◽  
Alan R. Cohen ◽  
Arun K. Gosain

The interplay of signals between dura mater, suture mesenchyme, and brain is essential in determining the fate of cranial sutures and the pathogenesis of premature suture fusion leading to craniosynostosis. At the forefront of research into suture fusion is the role of fibroblast growth factor and transforming growth factor–β, which have been found to be critical in the cell-signaling cascade involved in aberrant suture fusion. In this review, the authors discuss recent and ongoing research into the role of fibroblast growth factor and transforming growth factor–β in the etiopathogenesis of craniosynostosis.


2016 ◽  
Vol 2 (5) ◽  
pp. 248 ◽  
Author(s):  
Miguel Ángel Peña-Ortiz ◽  
Liliana Germán-Castelán ◽  
Aliesha González-Arenas

<p>Glioblastoma multiforme (GBM) is the most aggressive type of brain cancer, having the highest invasion, migration, proliferation, and angiogenesis rates. Several signaling pathways are involved in the regulation of these processes including growth factors and their tyrosine kinase receptors, such as vascular endothelial growth factor (VEGF), transforming growth factor beta (TGFβ), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), and insulin-like growth factor–I (IGF–I). Different kinases and regulators also participate in signaling pathways initiated by growth factors, such as mitogen-activated kinases (MAPK), protein kinases C (PKC), phosphatidylinositol-3 kinases (PI3K), protein kinase B (PKB or Akt), glycogen synthase kinase 3β (GSK3β), the mTOR complex, and Bcl-2. In this review, we will focus on the role of these proteins as possible therapeutic targets in GBM.</p>


2004 ◽  
Vol 279 (29) ◽  
pp. 30474-30479 ◽  
Author(s):  
Lucile Abécassis ◽  
Edith Rogier ◽  
Aimé Vazquez ◽  
Azzedine Atfi ◽  
Marie-Françoise Bourgeade

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