scholarly journals Homocysteine induces human mesangial cell apoptosis via the involvement of autophagy and endoplasmic reticulum stress

RSC Advances ◽  
2019 ◽  
Vol 9 (54) ◽  
pp. 31720-31727
Author(s):  
Shanshan Liang ◽  
Hua Liu ◽  
Sixiu Liu ◽  
Meng Wei ◽  
Fanfan Gao ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Endoplasmic Reticulum ◽  
Kidney Disease ◽  
Endoplasmic Reticulum Stress ◽  
Cell Apoptosis ◽  
Mesangial Cell ◽  
Progressive Increase ◽  
Human Mesangial Cell

Homocysteine (Hcy) level characterizes a progressive increase in chronic kidney disease (CKD).

scholarly journals Ligustrazine attenuates renal damage by inhibiting endoplasmic reticulum stress in diabetic nephropathy by inactivating MAPK pathways

RSC Advances ◽  
2018 ◽  
Vol 8 (39) ◽  
pp. 21816-21822 ◽  
Author(s):  
Hongling Yang ◽  
Shukun Wu
Keyword(s):  
Chronic Kidney Disease ◽  
Endoplasmic Reticulum ◽  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Endoplasmic Reticulum Stress ◽  
Renal Damage ◽  
Mapk Pathways ◽  
The World

Diabetic nephropathy (DN) is a major cause of chronic kidney disease around the world.

scholarly journals Endoplasmic reticulum stress inhibition attenuates hypertensive chronic kidney disease through reduction in proteinuria

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Zahraa Mohammed-Ali ◽  
Chao Lu ◽  
Mandeep K. Marway ◽  
Rachel E. Carlisle ◽  
Kjetil Ask ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Endoplasmic Reticulum ◽  
Kidney Disease ◽  
Endoplasmic Reticulum Stress

scholarly journals Huaier Extract Attenuates Acute Kidney Injury to Chronic Kidney Disease Transition by Inhibiting Endoplasmic Reticulum Stress and Apoptosis via miR-1271 Upregulation

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Jing-Ying Zhao ◽  
Yu-Bin Wu
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Endoplasmic Reticulum ◽  
Kidney Disease ◽  
Endoplasmic Reticulum Stress ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury

Endoplasmic reticulum stress (ERS) is strongly associated with acute kidney injury (AKI) to chronic kidney disease (CKD) transition. Huaier extract (HE) protects against kidney injury; albeit, the underlying mechanism is unknown. We hypothesized that HE reduces kidney injury by inhibiting ERS. In this study, using an AKI-CKD mouse model of ischemia-reperfusion injury (IRI), we evaluated the effect of HE on AKI-CKD transition. We also explored the underlying molecular mechanisms in this animal model and in the HK-2 human kidney cell line. The results showed that HE treatment improved the renal function, demonstrated by a significant decrease in serum creatinine levels after IRI. HE appreciably reduced the degree of kidney injury and fibrosis and restored the expression of the microRNA miR-1271 after IRI. Furthermore, HE reduced the expression of ERS markers glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) and inhibited apoptosis in the IRI group. This in vivo effect was supported by in vitro results in which HE inhibited apoptosis and decreased the expression of CHOP and GRP78 induced by ERS. We demonstrated that CHOP is a target of miR-1271. In conclusion, HE reduces kidney injury, probably by inhibiting apoptosis and decreasing the expression of GRP78 and CHOP via miR-1271 upregulation.

Abstract 656: N-acetylcystein Reduces Lipid Peroxidation and Advanced Glycation Related to Prevention of Macrophage Endoplasmic Reticulum Stress Induced by Albumin Isolated from Rats With Chronic Kidney Disease

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Juliana T Machado ◽  
Rodrigo T Iborra ◽  
Fernanda B Fusco ◽  
Gabriela Castilho ◽  
Raphael S Pinto ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Lipid Peroxidation ◽  
Endoplasmic Reticulum ◽  
Kidney Disease ◽  
Endoplasmic Reticulum Stress ◽  
Serum Albumin ◽  
Plasma Lipid ◽  
Lipid Peroxides ◽  
Advanced Glycation ◽  
The Impact

Objective: We analyzed the influence of N-acetylcysteine (NAC) in chronic kidney disease (CKD) rats on the plasma concentration of lipid peroxides (TBARS) and advanced glycation end products (AGE) and on the impact of serum CKD-albumin in the development of macrophage endoplasmic reticulum stress (ERS). Methods: CKD was induced by 5/6 nephrectomy in 2-month old male Wistar rats. Controls (C) were sham operated. Animals were treated or not with NAC (600mg/L of water). FPLC isolated serum albumin was purified by alchoolic extraction. J774 macrophages were incubated with serum albumin (1mg/mL; 18h) from all groups, and the expression of ERS markers (protein disulfide isomerase - PDI and Grp94 chaperone) determined by immunoblot. Comparisons were done by one-way ANOVA, Student t test. Results: After 60 days of CKD, body weight was 10% lower in CKD compared to C (p<0.01). This was prevented by NAC. Urea, creatinine, total cholesterol (TC), triglycerides (TG) (mg/dL), urinary protein excretion (mg/24h) (C, n= 31; C+NAC, n=20; CKD, n=74; CKD+NAC, n=32), total AGE and pentosidine (n= 8; fluorescence arbitrary unit) and TBARS (n= 7; nmoL/mL) were higher in CKD (122±8; 0.9±0.07; 151±6; 83±4; 46±2.5; 32620±673; 16700±1370; 6.6±0.5, respectively) and in CKD+NAC (91.4±5; 0.6±0.02; 126±7.5; 73±6; 51±3.5; 24,720±1,114; 10,080±748; 4.5±0.5, respectively) in comparison to C (41±0.9; 0.4±0.03; 76±2.7; 51.5±3; 14±0.9; 21,750±960; 5,314±129; 2±0.2, respectively; p<0.001) and C+NAC (40±0.9; 0.3±0.02; 76±2.6; 68±4; 18.4±1.5; 20,040±700; 5,050±267; 1.8±0.2, respectively; p<0,001). TC, urea, creatinine, total AGE, pentosidine and TBARS were respectively, 17%, 25%, 33%, 24%, 40% and 28% (p<0.01) lower in CKD+NAC, than in CKD. Glycemia was higher in C+NAC (107±4.6) and CKD+NAC (107±2.6) than in C (96±1.8; p<0.05) and CKD (98±1.6; p<0.01), respectively. In macrophages (n=6), CKD albumin increased PDI (5 and 7 times, p<0.01) and Grp94 (66% and 80%, p<0.01) in comparison to C and CKD+NAC-albumin treated cells, respectively. Conclusion: NAC reduces plasma lipid peroxidation and AGE and abrogates ERS induced by CKD-albumin. This may contribute to attenuate the deleterious effects of CKD-albumin on lipid accumulation in macrophages helping preventing atherogenesis in CKD.

scholarly journals Correlation of increased Th17/Treg cell ratio with endoplasmic reticulum stress in chronic kidney disease

Medicine ◽  
2018 ◽  
Vol 97 (20) ◽  
pp. e10748 ◽  
Author(s):  
Xiaojing Zhu ◽  
Shuiqin Li ◽  
Qiaona Zhang ◽  
Dan Zhu ◽  
Yang Xu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Endoplasmic Reticulum ◽  
Kidney Disease ◽  
Endoplasmic Reticulum Stress ◽  
Treg Cell ◽  
Cell Ratio
Sign in / Sign up

Export Citation Format

Share Document