scholarly journals Transforming growth factor beta-1 and vascular endothelial growth factor in the recovery and formation of skin scars

2021 ◽  
Vol 25 (3) ◽  
pp. 235-242
Author(s):  
Varvara G. Nikonorova ◽  
Vladimir V. Chrishtop ◽  
Tatyana A. Rumyantseva

Relevance. Scars are multi-tissue structures that significantly reduce the quality of life of the young, able-bodied population. The most socially significant variants are represented by hypertrophic and keloid postoperative scars and scars after burns, atrophic scars after acne vulgaris and striae. Growth factors, which are also used for their treatment, play a significant role in their formation and progression. The aim of this work is to summarize data on the participation of growth factors (transforming growth factor beta-1 and vascular endothelial growth factor) in the formation of a hypertrophic or atrophic scar. Materials and Methods. The study of literary sources of scientometric scientific bases was carried out. Results and Discussion . The study showed that the duration of the scarring phases preceding it is of great importance in scar formation, their prolongation leads to chronic inflammation and the attachment of an autoimmune component, an increase in the number of myofibroblasts due to inhibition of apoptosis and an increase in the synthesis of intercellular substance and immature forms of collagen, as well as thinning of the epidermis over scar. Growth factors such as growth factor beta-1 and vascular endothelial growth factor are capable of shifting the balance of these two main pathways or towards proliferative processes, contributing to an increase in the number of blood vessels in the hemomicrocirculatory bed, the number of mast cells and total cellularity, as well as, in some cases, the synthesis of keloid - that is, the formation of a hypertrophic or keloid scar. On the contrary, the prevalence of inflammatory processes leads to a decrease in cellularity, a decrease in blood vessels and intercellular substance, as well as damage to elastin and collagen fibers, forming the phenotype of an atrophic scar or striae. Conclusion. Growth factors play a key role in scar formation, contributing to an increase in the number of blood vessels in the hemomicrocirculatory bed, the number of mast cells and total cellularity, as well as, in some cases, the synthesis of keloid - that is, the formation of a hypertrophic or keloid scar.

2021 ◽  
Vol 12 (10) ◽  
Author(s):  
Chi-Ting Su ◽  
Tzu-Ming Jao ◽  
Zsolt Urban ◽  
Yue-Jhu Huang ◽  
Daniel H. W. See ◽  
...  

AbstractTransforming growth factor beta (TGFβ) signalling regulates extracellular matrix accumulation known to be essential for the pathogenesis of renal fibrosis; latent transforming growth factor beta binding protein 4 (LTBP4) is an important regulator of TGFβ activity. To date, the regulation of LTBP4 in renal fibrosis remains unknown. Herein, we report that LTBP4 is upregulated in patients with chronic kidney disease and fibrotic mice kidneys created by unilateral ureteral obstruction (UUO). Mice lacking the short LTBP4 isoform (Ltbp4S−/−) exhibited aggravated tubular interstitial fibrosis (TIF) after UUO, indicating that LTBP4 potentially protects against TIF. Transcriptomic analysis of human proximal tubule cells overexpressing LTBP4 revealed that LTBP4 influences angiogenic pathways; moreover, these cells preserved better mitochondrial respiratory functions and expressed higher vascular endothelial growth factor A (VEGFA) compared to wild-type cells under hypoxia. Results of the tube formation assay revealed that additional LTBP4 in human umbilical vein endothelial cell supernatant stimulates angiogenesis with upregulated vascular endothelial growth factor receptors (VEGFRs). In vivo, aberrant angiogenesis, abnormal mitochondrial morphology and enhanced oxidative stress were observed in Ltbp4S−/− mice after UUO. These results reveal novel molecular functions of LTBP4 stimulating angiogenesis and potentially impacting mitochondrial structure and function. Collectively, our findings indicate that LTBP4 protects against disease progression and may be of therapeutic use in renal fibrosis.


Sign in / Sign up

Export Citation Format

Share Document