Amin Hasanvand
1, Shadan Saberi
2*1 Department of Pharmacology and toxicology, Faculty of pharmacy, Lorestan University of Medical Sciences, Khorramabad, Iran.
2 Department of Physiology and Pharmacology, Kerman University of Medical Sciences, Kerman, Iran.
Abstract
Renal fibrosis (RF) is the final step in chronic kidney disease (CKD) that is represented by abundant extracellular matrix (ECM)
components, tubular atrophy and inflammatory cell infiltration. Renal failure results from a series of factors as follows; the activation
of cytokines due to the entrance of bioactive molecules of plasma to the tubulointerstitial space, the activation of signal molecules
such as transforming growth factor beta (TGF-β), connective tissue growth factor (CTGF), the activation of renin angiotensin
system (RAS) especially angiotensin II (Ang II), endothelin-1, other pro-inflammatory cytokines including tumor necrosis factor
alpha (TNF-α) and interleukin-1 (IL-1), and finally endothelial to mesenchymal transition. Among all factors, this review focuses
on RAS by considering the role of component of two axes of this system and mediators involved in RF. Ang II participates in many
chronic diseases such as hypertension and chronic heart disease. Moreover, ACE/Ang II/ATR axis exhibits a fibrogenic effect while
angiotensin (1-7) reveals both anti-fibrotic and fibrotic effects. However, most researchers believe in the renoprotective effect of
ACE2/Ang 1-7/MasR axis. The ratios of activities of these two axes determine the progression or inhibition of RF. Several signaling
pathways and cytokines play role in RF but TGF-β is the most important mediator. The existence of a feedback relationship between
TGF-β and RAS is considered in this study
Implication for health policy/practice/research/
medical education
Renal fibrosis (RF) is the final step in chronic kidney disease
(CKD) that is represented by abundant extracellular matrix
(ECM) components, tubular atrophy and inflammatory cell
infiltration. Renal failure results from a series of factors as
follows; the activation of cytokines due to the entrance of
bioactive molecules of plasma to the tubulointerstitial space,
the activation of signal molecules such as transforming growth
factor beta (TGF-β), connective tissue growth factor (CTGF),
the activation of renin angiotensin system (RAS) especially
angiotensin II, endothelin-1, other pro-inflammatory
cytokines including tumor necrosis factor alpha (TNF-α) and
interleukin-1 (IL-1), and finally endothelial to mesenchymal
transition.
Citation: Hasanvand A, Saberi S. Renin angiotensin system and different mediators induce renal fibrosis. J Renal Endocrinol. 2018;4:e09.
DOI:10.15171/jre.2018.09.