Angiotensin II receptor blocker inhibits tumour necrosis factor‐alpha‐induced cell damage in human renal proximal tubular epithelial cells

Kagawa, Tetsuya; Takao, Toshihiro; Horino, Taro; Matsumoto, Reiko; Inoue, Koh; Morita, Tatsuhito; Hashimoto, Kozo

doi:10.1111/j.1440-1797.2008.00918.x

Cited by 19 publications

(15 citation statements)

References 27 publications

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“…All of the components necessary for NADPH oxidase to function are present in the kidney, including the presence of four different isoforms of this oxidase-NOX1, NOX2, NOX4, and NOX5 (8,33,112). The expression of these different NADPH oxidase isoform components has been observed throughout the cortex and medulla of the mammalian (including human) kidney, including in the mesangium (97,136,184,190), proximal convoluted tubules, distal convoluted tubules, collecting duct, macula densa (17,77,139,217,281,309,322), endothelium, and VSMCs (8).…”

Section: Nadph Oxidase Rosmentioning

confidence: 99%

Oxidant Mechanisms in Renal Injury and Disease

Ratliff

Abdulmahdi

Pawar

et al. 2016

Antioxidants & Redox Signaling

533

513

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Significance: A common link between all forms of acute and chronic kidney injuries, regardless of species, is enhanced generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) during injury/ disease progression. While low levels of ROS and RNS are required for prosurvival signaling, cell proliferation and growth, and vasoreactivity regulation, an imbalance of ROS and RNS generation and elimination leads to inflammation, cell death, tissue damage, and disease/injury progression. Recent Advances: Many aspects of renal oxidative stress still require investigation, including clarification of the mechanisms which prompt ROS/ RNS generation and subsequent renal damage. However, we currently have a basic understanding of the major features of oxidative stress pathology and its link to kidney injury/disease, which this review summarizes. Critical Issues: The review summarizes the critical sources of oxidative stress in the kidney during injury/ disease, including generation of ROS and RNS from mitochondria, NADPH oxidase, and inducible nitric oxide synthase. The review next summarizes the renal antioxidant systems that protect against oxidative stress, including superoxide dismutase and catalase, the glutathione and thioredoxin systems, and others. Next, we describe how oxidative stress affects kidney function and promotes damage in every nephron segment, including the renal vessels, glomeruli, and tubules. Future Directions: Despite the limited success associated with the application of antioxidants for treatment of kidney injury/disease thus far, preventing the generation and accumulation of ROS and RNS provides an ideal target for potential therapeutic treatments. The review discusses the shortcomings of antioxidant treatments previously used and the potential promise of new ones.

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Section: Nadph Oxidase Rosmentioning

confidence: 99%

Oxidant Mechanisms in Renal Injury and Disease

Ratliff

Abdulmahdi

Pawar

et al. 2016

Antioxidants & Redox Signaling

533

513

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“…Regardless of its renal or extrarenal origin, angiotensin II acting via Agtr1 has been implicated in pronephrotic changes similar to those detected in the kidney of diabetic ZDF rats. Thus, in addition to the well-established link between angiotensin II and the NF-kB-dependent NOX activation and ROS production (40, 41), Agtr1 activation has been shown to reduce plasma adiponectin (42), down-regulate adipoR1 (43), increase the plasma uric acid (44) and IL-18 (45), increase the gene expression of Il-6 (46) and TNF-α (47), and increase caspase 3/7 activity in kidney tissue (48).…”

Section: Discussionmentioning

confidence: 99%

Overactive cannabinoid 1 receptor in podocytes drives type 2 diabetic nephropathy

Jourdan¹,

Szanda²,

Rosenberg

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

107

145

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Diabetic nephropathy is a major cause of end-stage kidney disease, and overactivity of the endocannabinoid/cannabinoid 1 receptor (CB 1 R) system contributes to diabetes and its complications. Zucker diabetic fatty (ZDF) rats develop type 2 diabetic nephropathy with albuminuria, reduced glomerular filtration, activation of the reninangiotensin system (RAS), oxidative/nitrative stress, podocyte loss, and increased CB 1 R expression in glomeruli. Peripheral CB 1 R blockade initiated in the prediabetic stage prevented these changes or reversed them when animals with fully developed diabetic nephropathy were treated. Treatment of diabetic ZDF rats with losartan, an angiotensin II receptor-1 (Agtr1) antagonist, attenuated the development of nephropathy and down-regulated renal cortical CB 1 R expression, without affecting the marked hyperglycemia. In cultured human podocytes, CB 1 R and desmin gene expression were increased and podocin and nephrin content were decreased by either the CB 1 R agonist arachydonoyl-2′-chloroethylamide, angiotensin II, or high glucose, and the effects of all three were antagonized by CB 1 R blockade or siRNA-mediated knockdown of CNR1 (the cannabinoid type 1 receptor gene). We conclude that increased CB 1 R signaling in podocytes contributes to the development of diabetic nephropathy and represents a common pathway through which both hyperglycemia and increased RAS activity exert their deleterious effects, highlighting the therapeutic potential of peripheral CB 1 R blockade.iabetic nephropathy, a highly prevalent and serious complication of both type 1 and type 2 diabetes mellitus and a leading cause of renal failure, is characterized by albuminuria, decreased glomerular filtration rate (GFR), mesangial expansion, thickening of the glomerular basement membrane, and glomerular sclerosis (1). Multiple mechanisms have been implicated in the development of diabetic nephropathy, including activation of the renin-angiotensin system (RAS) (2), increase in oxidative (3) and nitrosative/nitrative stress (4), as well as an increase in local inflammation (5).The endocannabinoid system plays a well-documented role in obesity and its metabolic complications, including insulin resistance and type 2 diabetes (T2DM). Globally acting cannabinoid 1 receptor (CB 1 R) antagonists/inverse agonists improve obesity-related insulin resistance, dyslipidemia, fatty liver, and β-cell loss, and attenuate obesity-related inflammatory changes both in preclinical models of diet-induced or genetic obesity and in clinical trials in overweight subjects with metabolic syndrome (reviewed in refs. 6 and 7). Global CB 1 R blockade also has beneficial effects in mouse models of type 1 and type 2 diabetic nephropathy (8-11). However, the therapeutic development of this class of compounds has been halted because of adverse neuropsychiatric side effects in a small proportion of treated subjects (12). Recent studies in rodent models have demonstrated that peripherally restricted CB 1 R antagonists are as effective as globally acti...

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“…EGF, epidermal growth factor; LDL, low-density lipoprotein; IL-1, interleukin 1; TNF-␣, tumor necrosis factor-␣; LPS, lipopolysaccharide; 5HT, 5-hydroxy tryptophan; VEGF, vascular endothelial growth factor; MEK, MAPK kinase; TGF-1␤, transforming growth factor-1␤; PKC, protein kinase C; ET1, endothelin 1; DAG, diacylglycerol; JAK, Janus-associated kinase; STAT-1␣, signal transducers and activators of transcription-1␣; AP-1, activator protein; Sp-1, selective promoter factor; PLA 2 , phospholipase A 2 ; Ca 2ϩ , calcium; AA, arachidonic acid; PDE4, phosphodiesterase 4; cAMP, cyclic adenosine monophosphate; PKA, protein kinase A; AGE, advanced glycation pathways; RAGE, receptor for AGE; cGMP, cyclic guanosine monophosphate. 139,148,342,366) (Fig. 6).…”

Section: Nistala Et Al 2062mentioning

confidence: 99%