«The present study has shown, for the first time, the expression of (P)RR in human breast carcinoma tissues and cultured breast carcinoma cell lines. These findings have raised the possibility that the blockade of the (P)RR signaling may be a novel therapeutic strategy against breast carcinomas.» 

(Ohba et al. 2014)

«Overall, this study contributes to the emerging but exciting literature on the role of both canonical (Ang II/AGTR1) and non-canonical (Ang II-independent (P)RR signalling) RAS activation in tumourigenesis. As such, the (P)RR has the potential to be an ideal target for the development of new anti-cancer therapies.» 

(Delforce et al. 2016)

«This is the first evidence that the PRR has an important role in development of glioma by aberrant activation of the Wnt/ß-catenin signaling pathway. This receptor may be both a prognostic marker and a therapeutic target for gliomas of all grades.»

(Kouchi et al. 2017)

«ATP6AP2 promotes cell cycle progression, mitosis  and proliferation and inhibits differentiation and ciliogenesis. Although many details still need to be elucidated, our data suggest that ATP6AP2 is indispensable for cell cycle progression and that the protein prevents cell cycle exit and ciliogenesis, thereby enabling cells to enter differentiation. The novel link between ATP6AP2 and the cell cycle suggests an important role for this protein in stem cell proliferation and differentiation, as well as in tumourigenesis.» 

(Wanka et al. 2017)

«The experimental data confirmed the pivotal role of the receptor in cell surface generation of angiotensin and suggested its potential role in tissue fibrosis via receptor activation and intracellular signaling. The data also questioned the ability of soon available renin inhibitors to inhibit the activity of receptor-bound renin and prorenin, and the benefit of a new class of drug -- (pro)renin receptor blockers -- to prevent tissue damage.» 

(Nguyen 2007)

«These and the numerous other genes involved in proinflammatory and profibrotic processes contained within the (pro)renin genetic program suggest that blockade of both angiotensin II and (pro)renin receptor binding may be optimal for complete attenuation of organ damage.» 

(Melnyk et al. 2009)

«Moreover, our results provide the direct experimental in vivo evidence that (P)RR blockers may display additional cardiac effects on top of effective RAS blockade, because (P)RR activation induced distinct Ang II-independent extracellular matrix remodeling and worsening of cardiac function. (P)RR blockers may allow more complete myocardial protection in combination of effective AT1 receptor blockade and prevent the deleterious Ang II-independent actions of renin that are not inhibited by renin inhibitors.» 

(Moilanen et al. 2012)

«These findings suggest that (P)RR contributes to pressure/volume regulation in HF (heart failure) and identifies the receptor as a potential therapeutic target in this disease.» 

(Rademaker et al. 2012)

«As current treatment of cardiovascular and renal diseases with RAS-blocking agents does not fully abolish end-organ damage, there is hope that blockage of PRR would prevent organ damage.»

(Raymond et al. 2013)

«This study advances our understanding of the mechanisms involved in the pathophysiology of renal disease and suggests (pro)renin receptor as a potential target for management of this common clinical problem.» 

(Huang et al. 2013)

«In summary, our results indicated that enhanced PRR expression plays an important role in high glucose induced podocytes structural and functional abnormalities. Decreased expression or activity of PRR in podocytes might be important for reversal of high glucose related podocyte damage.»

(Li et al 2014)

«Our data highlights the potential beneficial effects of (P)RR blockade on obesity and its related-cardiometabolic complications. As such, it suggests that it may be a novel preventive and therapeutic avenue for the metabolic syndrome in the future.» 

(Tan  et al. 2014)

«[...] high glucose-induced up-regulation of PRR plays an important role in reduction of autophagy and enhanced apoptosis in podocytes. PI3K-AKT-mTOR-ULK1 signaling pathway mediates the PRR effects. These findings may help develop a new therapeutic strategy for management of podocytes injury in diabetes.» 

(Li et al. 2015)

«The present study found that (P)RR-blockade post-MI in mice ameliorates infarct size, cardiac fibrosis/hypertrophy and cardiac dysfunction, and identifies the receptor as a potential therapeutic target in this setting.» 

(Ellmers et al. 2016)

«Targeting PRR [...] may offer a new intervention for management of high fructose-induced salt-sensitive hypertension » 

(Xu et al. 2017)

«We conclude that PRR can promote kidney injury and fibrosis by amplifying Wnt/ß-catenin signaling.» 

(Li et al. 2017)

«The present study has raised the possibility that (P)RR is a novel target for the development of the new therapies, not only in cardiovascular, renal diseases including diabetic nephropathy, but also in proliferative diseases including cancers.» 

(Ohba et al. 2013)