Version 1
: Received: 30 April 2023 / Approved: 1 May 2023 / Online: 1 May 2023 (04:12:22 CEST)
How to cite:
Atiakshin, D.; Morozov, S.; Dlin, V.; Kostin, A.; Ignatyuk, M.; Kuzovleva, G.; Baiko, S.; Buchwalow, I.; Tiemann, M. Renal Mast Cell Specific Proteases in the Pathogenesis of Tubulointerstitial Fibrosis: Case Report. Preprints2023, 2023050013. https://doi.org/10.20944/preprints202305.0013.v1
Atiakshin, D.; Morozov, S.; Dlin, V.; Kostin, A.; Ignatyuk, M.; Kuzovleva, G.; Baiko, S.; Buchwalow, I.; Tiemann, M. Renal Mast Cell Specific Proteases in the Pathogenesis of Tubulointerstitial Fibrosis: Case Report. Preprints 2023, 2023050013. https://doi.org/10.20944/preprints202305.0013.v1
Atiakshin, D.; Morozov, S.; Dlin, V.; Kostin, A.; Ignatyuk, M.; Kuzovleva, G.; Baiko, S.; Buchwalow, I.; Tiemann, M. Renal Mast Cell Specific Proteases in the Pathogenesis of Tubulointerstitial Fibrosis: Case Report. Preprints2023, 2023050013. https://doi.org/10.20944/preprints202305.0013.v1
APA Style
Atiakshin, D., Morozov, S., Dlin, V., Kostin, A., Ignatyuk, M., Kuzovleva, G., Baiko, S., Buchwalow, I., & Tiemann, M. (2023). Renal Mast Cell Specific Proteases in the Pathogenesis of Tubulointerstitial Fibrosis: Case Report. Preprints. https://doi.org/10.20944/preprints202305.0013.v1
Chicago/Turabian Style
Atiakshin, D., Igor Buchwalow and Markus Tiemann. 2023 "Renal Mast Cell Specific Proteases in the Pathogenesis of Tubulointerstitial Fibrosis: Case Report" Preprints. https://doi.org/10.20944/preprints202305.0013.v1
Abstract
Kidney fibrosis is a complex polyetiological progressive disease manifesting as an intraorgan proliferation of the connective tissue with the appearance of cicatricial changes. However, pathogenetic mechanisms of renal fibrosis remain poorly understood. The paper highlights features of the protease phenotype and histotopography of mast cells (MCs) found in the kidney, as the key players in extracellular matrix remodeling in nephrofibrosis, detected in a patient diagnosed with "nephrosclerosis with the non-functioning upper pole of the duplex right kidney in the junction of refluxing megaureter of the upper pole of the duplex right kidney". The highest content of MCs was found in the kidney areas with fibrotic changes. MCs were actively involved in the development of inflammatory and fibrotic changes in limited loci of the specific tissue microenvironment of the kidney through targeted secretion of tryptase, chymase, and carboxypeptidase A3 to the vascular endothelium, nephron epithelium, interstitium cells, and components of the intercellular substance. The formation of a profibrotic environment in the kidney interstitium was facilitated by epigenetic effects of tryptase promoting epithelial-mesenchymal transition (EMT) of the nephron epithelium. A selectively increased number and targeted secretory activity of MCs in limited loci of the kidney parenchyma without visible pathological changes evidence a trigger pathogenetic role of specific proteases in the formation of a local microenvironment with a profibrogenic metabolic profile. Thus, MCs are actively involved in the mechanisms of formation and evolution of fibrogenic niches in the kidney; this fact can be used to develop new strategies for therapeutic options of tubulointerstitial fibrosis resulted from chronic kidney injury. Further study of the molecular phenotype of mast cells reveals new fundamental mechanisms of fibrosis pathogenesis being a significant tool for personalized therapy in nephrology.
Medicine and Pharmacology, Gastroenterology and Hepatology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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