Up-Regulation of SIRT1 Reduces Endoplasmic Reticulum Stress and Renal Fibrosis

Nephron ◽  
2016 ◽  
Vol 133 (2) ◽  
pp. 116-128 ◽  
Author(s):  
Jai Won Chang ◽  
Hyosang Kim ◽  
Chung Hee Baek ◽  
Raymond Bok Lee ◽  
Won Seok Yang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Renal Fibrosis

scholarly journals Inhibition of Reticulon-1A–Mediated Endoplasmic Reticulum Stress in Early AKI Attenuates Renal Fibrosis Development

2017 ◽  
Vol 28 (7) ◽  
pp. 2007-2021 ◽  
Author(s):  
Ying Fan ◽  
Wenzhen Xiao ◽  
Kyung Lee ◽  
Fadi Salem ◽  
Jiejun Wen ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Renal Fibrosis

scholarly journals A mouse model for inherited renal fibrosis associated with endoplasmic reticulum stress

2017 ◽  
Vol 10 (6) ◽  
pp. 773-786 ◽  
Author(s):  
Sian E. Piret ◽  
Eric Olinger ◽  
Anita A. C. Reed ◽  
M. Andrew Nesbit ◽  
Tertius A. Hough ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mouse Model ◽  
Renal Fibrosis

scholarly journals Chemical chaperon 4-phenylbutyrate protects against the endoplasmic reticulum stress-mediated renal fibrosis in vivo and in vitro

Oncotarget ◽  
2016 ◽  
Vol 7 (16) ◽  
pp. 22116-22127 ◽  
Author(s):  
Shing-Hwa Liu ◽  
Ching-Chin Yang ◽  
Ding-Cheng Chan ◽  
Cheng-Tien Wu ◽  
Li-Ping Chen ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Renal Fibrosis

scholarly journals Targeted inhibition of endoplasmic reticulum stress: New hope for renal fibrosis

2017 ◽  
Vol 16 (2) ◽  
pp. 1014-1020 ◽  
Author(s):  
Ben Ke ◽  
Na Zhu ◽  
Fuli Luo ◽  
Yang Xu ◽  
Xiangdong Fang
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Renal Fibrosis ◽  
Targeted Inhibition

scholarly journals Endoplasmic Reticulum Stress Implicated in the Development of Renal Fibrosis

2011 ◽  
Vol 17 (11-12) ◽  
pp. 1295-1305 ◽  
Author(s):  
Chih-Kang Chiang ◽  
Shih-Ping Hsu ◽  
Cheng-Tien Wu ◽  
Jenq-Wen Huang ◽  
Hui-Teng Cheng ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Renal Fibrosis

MiR-185-5p ameliorates endoplasmic reticulum stress and renal fibrosis by downregulation of ATF6

2020 ◽  
Vol 100 (11) ◽  
pp. 1436-1446 ◽  
Author(s):  
Quan Yuan ◽  
Tianhua Xu ◽  
Ying Chen ◽  
Wei Qu ◽  
Dan Sun ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Renal Fibrosis

scholarly journals AIM2 Inflammasome Contributes to Aldosterone-induced Renal Injury via Endoplasmic Reticulum Stress

2021 ◽  
Author(s):  
Yong Wu ◽  
Huan Yang ◽  
Sujuan Xu ◽  
Ming Cheng ◽  
Jie Gu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Endoplasmic Reticulum ◽  
Kidney Disease ◽  
Endoplasmic Reticulum Stress ◽  
Renal Injury ◽  
Renal Fibrosis ◽  
Inflammasome Activation ◽  
Mineralocorticoid Receptor Antagonist

Inflammatory response and renal fibrosis are the hallmarks of chronic kidney disease (CKD). However, the specific mechanism of aldosterone-induced renal injury in the progress of CKD requires elucidation. Emerging evidence has demonstrated that absent in melanoma 2 (AIM2)-mediated inflammasome activation and endoplasmic reticulum stress (ERS) play a pivotal role in the renal fibrosis. Here, we investigated whether overexpression or deficiency of AIM2 affects ERS and fibrosis in aldosterone-infused renal injury. Interestingly, we found that AIM2 was markedly expressed in the diseased proximal tubules from human and experimental chronic kidney disease. Mechanically, overactivation of AIM2 aggravated aldosterone-induced ERS and fibrotic changes in vitro while knockdown of AIM2 blunted these effects in vivo and vitro. By contrast, AIM2 deficiency ameliorated renal structure and function deterioration, decreased proteinuria levels and lower systolic blood pressure in vivo; silencing of AIM2 blocked inflammasome-mediated signaling pathway, relieved ERS and fibrotic changes in vivo. Furthermore, mineralocorticoid receptor antagonist eplerenone and ERS inhibitor tauroursodeoxycholic acid (TUDCA) had nephroprotective effects on the basis of AIM2 overactivation in vitro while they failed to produce a more remarkable reno-protective effect on the treatment of AIM2 silence in vitro. Notably, the combination of TUDCA with AIM2 knockdown significantly reduced proteinuria levels in vivo. Additionally, immunofluorescence assay identified that apoptosis-associated speck-like protein (ASC) recruitment and Gasdermin-D (GSDMD) cleavage respectively occurred in the glomeruli and tubules in vivo. These findings establish a crucial role for AIM2 inflammasome in aldosterone-induced renal injury, which may provide a novel therapeutic target for the pathogenesis of CKD.

scholarly journals Mito-TEMPO Alleviates Renal Fibrosis by Reducing Inflammation, Mitochondrial Dysfunction, and Endoplasmic Reticulum Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Yuqing Liu ◽  
Yundan Wang ◽  
Wei Ding ◽  
Yingdeng Wang
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Endoplasmic Reticulum ◽  
Kidney Disease ◽  
Endoplasmic Reticulum Stress ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Renal Fibrosis ◽  
Oxidative Stress Markers ◽  
Stress Markers

Background. Renal fibrosis is a common pathological symptom of chronic kidney disease (CKD). Many studies support that mitochondrial dysfunction and endoplasmic reticulum (ER) stress are implicated in the pathogenesis of CKD. In our study, we investigated the benefits and underlying mechanisms of Mito-TEMPO on renal fibrosis in 5/6 nephrectomy mice. Methods. Mice were randomly divided into five groups as follows: control group, CKD group, CKD + Mito-TEMPO (1 mg·kg−1·day−1) group, CKD + Mito-TEMPO (3 mg·kg−1·day−1) group, and Mito-TEMPO group (3 mg·kg−1·day−1). Renal fibrosis was evaluated by PAS, Masson staining, immunohistochemistry, and real-time PCR. Oxidative stress markers such as SOD2 activity and MDA level in serum and isolated mitochondria from renal tissue were measured by assay kits. Mitochondrial superoxide production was evaluated by MitoSOX staining and Western blot. Mitochondrial dysfunction was assessed by electron microscopy and real-time PCR. ER stress-associated protein was measured by Western blot. Results. Impaired renal function and renal fibrosis were significantly improved by Mito-TEMPO treatment. Furthermore, inflammation cytokines, profibrotic factors, oxidative stress markers, mitochondrial dysfunction, and ER stress were all increased in the CKD group. However, these effects were significantly ameliorated in the Mito-TEMPO treatment group. Conclusions. Mito-TEMPO ameliorates renal fibrosis by alleviating mitochondrial dysfunction and endoplasmic reticulum stress possibly through the Sirt3-SOD2 pathway, which sheds new light on prevention of renal fibrosis in chronic kidney disease.

Abstract #403: The Glutathione Mimic Ebselen Inhibits Oxidative Stress but not Endoplasmic Reticulum Stress in Endothelial Cells.

2015 ◽  
Vol 21 ◽  
pp. 85-86
Author(s):  
William Kurban ◽  
Salma Makhoul Ahwach ◽  
Melanie Thomas ◽  
Luisa Onsteed-Haas ◽  
Michael Haas
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress
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