Corpus ID: 23084693

NOX , RAS and PKC-Δ as Key Players in Kidney Diseases : A Possible Role of Rottlerin

@inproceedings{Chhiber2015NOXR,
  title={NOX , RAS and PKC-$\Delta$ as Key Players in Kidney Diseases : A Possible Role of Rottlerin},
  author={Nirlep Chhiber and T. Kaur and S. Singla},
  year={2015}
}
ROS: Reactive Oxygen Species; RAS: Renin Angiotensin System; PKC-Δ: Protein Kinase C-Δ; NOX: NADPH Oxidase; BK Channels: Ca2+ Activated Potassium Channels; RAAS: Renin Angiotensin Aldosterone System; Caox: Calcium Oxalate; ACE2: Angiotensin-Converting Enzyme 2; Ang II: Angiotensin II; EMT: Epithelial To Mesenchymal Transition; AT1R :Ang II Type 1 Receptor; CKD: Chronic Kidney Disease; L-NAME: Nω-Nitro-LArginine Methyl Ester; AGE: Advanced Glycation End Products; ESRD: End Stage Renal Disease… Expand

Figures and Tables from this paper

References

SHOWING 1-10 OF 65 REFERENCES
Involvement of renin–angiotensin–aldosterone system in calcium oxalate crystal induced activation of NADPH oxidase and renal cell injury
TLDR
Results indicate that hyperoxaluria-induced production of ROS, injury and inflammation are in part associated with the activation of Nox through renin–angiotensin–aldosterone pathway. Expand
Nox-4 and progressive kidney disease
TLDR
The role of Nox-4 as a target for renoprotection remains controversial, although recent positive preclinical data have stimulated increased interest in inhibiting the enzyme in clinical trials of renal disease. Expand
Oxidative stress and glomerular filtration barrier injury: role of the renin-angiotensin system in the Ren2 transgenic rat.
TLDR
Reductions in blood pressure, albuminuria, and tissue oxidative stress with AT1R blockade were associated with improved indexes of glomerular filtration barrier integrity and renal RAS in Ren2 rats. Expand
Role of Angiotensin II type 1 receptor on renal NAD(P)H oxidase, oxidative stress and inflammation in nitric oxide inhibition induced-hypertension.
TLDR
No induced-hypertension is associated with up-regulation of NADPH oxidase, oxidative stress production and overexpression of key inflammatory mediators, as evidenced by their reversal with AT1R blocker treatment. Expand
Albumin overload activates intrarenal renin–angiotensin system through protein kinase C and NADPH oxidase-dependent pathway
TLDR
Examination of the intracellular signal pathway involved in albumin-triggered activation of the intrarenal renin–angiotensin system found chronic inhibition of NADPH oxidase by apocynin largely ameliorated intrarenals activation of RAS. Expand
NADPH oxidases and angiotensin II receptor signaling
TLDR
The mechanism of activation of NADPH oxidases by Ang II is summarized and the molecular targets of ROS in Ang II signaling in the vasculature, kidney and brain are described. Expand
Role of NADPH Oxidase-Mediated Reactive Oxygen Species in Podocyte Injury
TLDR
This review focuses on the mechanism of NAD PH oxidase-mediated ROS in podocyte injury under different pathophysiological conditions and the therapeutic perspectives of NADPH oxidase in kidney diseases related to Podocyte injury. Expand
Reactive oxygen species as mediators of angiotensin II signaling
TLDR
Future work will be directed towards identifying other important redox-sensitive signaling pathways and their relationship to the physiology and pathophysiology of the renin-angiotensin system. Expand
Role of Superoxide in Modulating the Renal Effects of Angiotensin II
TLDR
Some of the acute renal effects of angiotensin II may be enhanced by an increased NADPH oxidase-derived O2− production that reduces renal NO bioavailability. Expand
ACE2 deficiency increases NADPH‐mediated oxidative stress in the kidney
TLDR
It is demonstrated that genetic deficiency of ACE2 activity in mice fosters oxidative stress in the kidney in the absence of overt hypertension and is associated with reduced kidney capacity to hydrolyze Ang II. Expand
...
1
2
3
4
5
...