Connexin-Based Channels and RhoA/ROCK Pathway in Angiotensin II-Induced Kidney Damage

Abstract

The incidence of chronic kidney diseases is increasing worldwide, and there is no efficient therapy to reduce this phenomenon. The main therapies currently available focus on the control of blood pressure and the optimization of the blockade of the renin-angiotensin system (RAS). In addition, it is known that in several models of kidney damage, the amounts of connexins are altered. On the other hand, fasudil, a selective ROCK blocker, has shown renoprotective effects. The beneficial effects of blocking the RhoA/ROCK pathway in renal function may be related to its action of reducing macrophage infiltration, inflammation, and oxidative stress (OS), its expression of extracellular matrix genes and proteinuria, or to its effects on connexin abundance. Even though a correlation has been found between renal damage, caused by an increase in the RAS activity, connexins, and the RhoA/ROCK signaling pathway, it has not yet been possible to clearly determine its functional significance. Moreover, it has not been possible to identify the preponderance of this signaling pathway in the development of chronic kidney diseases. Here, we describe the advances in this subject.