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Role of the Intrarenal Renin Angiotensin System in Inflammation and Fibrosis in Experimental Models of Kidney Disease

Call for Papers

Despite the role of the intrarenal renin angiotensin system (RAS) in arterial blood pressure regulation it also has a pathophysiologic role in the development of tubular and interstitial fibrosis, glomerulonephritis (GN), and other pathologies. Angiotensin II (Ang II) is the final effector of the RAS. Ang II activates intracellular signaling pathways leading to inflammation, cell growth, induction of profibrotic factors, and so on. Ang II also induces proinflammatory factors through the Ang II type 1 (AT1) receptor that contributes to renal damage. Although there is increasing evidence about the role of the RAS in proinflammatory mediators, crosstalk among RAS and inflammatory mediators is not fully understood. Good examples are the regulation of renal angiotensinogen by inflammatory mediators and the role of the prorenin receptor in fibrosis, among others. There are still several models of kidney disease in which these profiles are not investigated. The main challenge of this special issue is to understand the mechanisms of kidney injury through the comprehensive understanding of the interactions between the RAS and inflammatory mediators. We especially welcome submissions related to experimental models of kidney disease focused on the subject mentioned above. We also encourage submissions of review articles describing the current state of the art.

Potential topics include but are not limited to the following:

  • Intrarenal renin angiotensin system and glomerulonephritis
  • Intrarenal renin angiotensin system and tubulointerstitial fibrosis in experimental models of kidney disease or hypertension
  • Regulation of proinflammatory mediators by intrarenal renin angiotensin system
  • Regulation of intrarenal renin angiotensin system by proinflammatory mediators
  • Crosstalk between proinflammatory mediators and the intrarenal renin angiotensin system
  • Descriptive studies about the expression of the components of the renin angiotensin system in animal models of kidney disease
  • Angiotensin-(1–7)/angiotensin-converting enzyme 2/MAS receptor axis as a pharmacological tool intervention on the intrarenal renin angiotensin system and proinflammatory mediators

Authors can submit their manuscripts through the Manuscript Tracking System at

Submission DeadlineFriday, 23 March 2018
Publication DateAugust 2018

Papers are published upon acceptance, regardless of the Special Issue publication date.

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