Attenuation of diabetic nephropathy in diabetes rats induced by streptozotocin by regulating the endoplasmic reticulum stress inflammatory response

Qi, Wei; Mu, Jian; Luo, Zhigang; Zeng, Wei; Guo, Yang; Pang, Qian; Ye, Zi-Lin; Liu, Li; Yuan, Fang; Feng, Bo

doi:10.1016/j.metabol.2010.07.021

Cited by 93 publications

(60 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ER stress can be induced by glucose, glucosamine, and oxidative stress, factors known to induce fibroproliferative remodeling in multiple tissues (5,9,10). Chemical chaperones that reduce ER stress, such as valproate and 4-phenylbutyrate, reduce atherosclerosis and fibrosis (3,(11)(12)(13) and also inhibit TGF-␤-induced type I collagen production independent of Smad reporter activity (14).…”

Section: Endoplasmic Reticulum (Er)mentioning

confidence: 99%

Calreticulin Regulates Transforming Growth Factor-β-stimulated Extracellular Matrix Production

Zimmerman

Graham²,

Pallero

et al. 2013

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Endoplasmic reticulum (ER) stress is associated with fibrotic diseases, although the mechanisms are not completely understood. Results: The ER stress protein calreticulin regulates TGF-␤ stimulated extracellular matrix through control of intracellular calcium and NFAT signaling. Conclusion: Calreticulin is necessary for TGF-␤ stimulated extracellular matrix production. Significance: These findings identify calreticulin as a mechanistic link between ER stress and fibrosis.

show abstract

Section: Endoplasmic Reticulum (Er)mentioning

confidence: 99%

Calreticulin Regulates Transforming Growth Factor-β-stimulated Extracellular Matrix Production

Zimmerman

Graham²,

Pallero

et al. 2013

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Though we successfully established a mice model with nephropathy and observed the upregulated GRP78 and CHOP in this model, we were not able to directly prove that ER stress did participate in the renal lesion of diabetes. Some study has proved that ER stress contributed to the renal injury in diabetic rats induced by STZ 10,21,22 , thus we conjecture that both models share the same mechanism on the onset of DN. We believe that this mechanism on DN can be explored by inhibiting the ER stress using an ER stress inhibitors such as 4-phenylbutyric acid (4-PBA).…”

Section: Discussionmentioning

confidence: 68%

Endoplasmic reticulum stress and renal lesion in mice with combination of high-fat diet and streptozotocin-induced diabetes

Xie

Liu

et al. 2016

Acta Cir. Bras.

View full text Add to dashboard Cite

PURPOSE:To investigate in the kidney the pathologic changes and expression of GRP78 and CHOP in the Kunming (KM) mice with combination of high-fat diet and streptozotocin-induced diabetes. METHODS:Sixty two male KM mice were randomly divided into a normal control (NC) group (n=20) and a high-fat diet (HFD) group (n=42). After a four-week dietary manipulation, the KM mice in the HFD group were injected intraperitoneally with streptozotocin to induce diabetes. After diabetic models were successfully established, the kidneys were excised and conserved for further test. RESULTS:No significant difference in the body weight was observed after the dietary manipulation (p=0.554). After the streptozotocin was injected, fasting blood glucose levels in the diabetes group (DM) were significantly higher than that in the NC group (p<0.0001).Glomerular atrophy observed under light microscope in the DM group was more serious compared with the NC group. The expression of GRP78 and CHOP in the kidneys of the mice in the DM group were higher compared with the NC group. CONCLUSION:Renal lesion occurs in the diabetic Kunming mice induced by combination of high-fat diet and low-dose streptozotocin, and endoplasmic reticulum stress and CHOP may contribute to the injury process.

show abstract

“…Small-molecule chemical chaperones such as TUDCA and 4-PBA are suspected to enhance either protein secretion or the folding capacity of the ER (Park & Ozcan 2013). Indeed, recent work on experimental models of DN has demonstrated that 4-PBA (Qi et al 2011) and TUDCA (Chen et al 2008, Fang et al 2013 could potentially slow the progression of DN through the attenuation of ER stress-induced apoptosis via the reduction of GRP78 and PERK expression, and the restoration of defective autophagy. However, it is not yet understood whether chemical chaperones could directly improve kidney function or whether these results are simply confounded by the improvement in glycaemic control observed with this class of agents.…”

Section: Therapeutic Implications Of Er Stress Modulatorsmentioning

confidence: 99%

Stress in the kidney is the road to pERdition: is endoplasmic reticulum stress a pathogenic mediator of diabetic nephropathy?

Zhuang¹,

Forbes²

2014

Journal of Endocrinology

View full text Add to dashboard Cite

The endoplasmic reticulum (ER) is an organelle that primarily functions to synthesise new proteins and degrade old proteins. Owing to the continual and variable nature of protein turnover, protein synthesis is inherently an error-prone process and is therefore tightly regulated. Fortunately, if this balance between synthesis and degradation is perturbed, an intrinsic response, the unfolded protein response (UPR) is activated to restore ER homoeostasis through the action of inositol-requiring protein 1, activating transcription factor 6 and PKR-like ER kinase transmembrane sensors. However, if the UPR is oversaturated and misfolded proteins accumulate, the ER can shift into a cytotoxic response, a physiological phenomenon known as ER stress. The mechanistic pathways of the UPR have been extensively explored; however, the role of this process in such a synthetic organ as the kidney requires further clarification. This review will focus on these aspects and will discuss the role of ER stress in specific resident kidney cells and how this may be integral in the pathogenesis and progression of diabetic nephropathy (DN). Given that diabetes is a perturbed state of protein turnover in most tissues, it is important to understand if ER stress is a secondary or tertiary response to other changes within the diabetic milieu or if it is an independent accelerator of kidney disease. Modulators of ER stress could provide a valuable tool for the treatment of DN and are under active investigation in other contexts. Key Words" endoplasmic reticulum stress " diabetic nephropathy

show abstract

Attenuation of diabetic nephropathy in diabetes rats induced by streptozotocin by regulating the endoplasmic reticulum stress inflammatory response

Cited by 93 publications

References 41 publications

Calreticulin Regulates Transforming Growth Factor-β-stimulated Extracellular Matrix Production

Calreticulin Regulates Transforming Growth Factor-β-stimulated Extracellular Matrix Production

Endoplasmic reticulum stress and renal lesion in mice with combination of high-fat diet and streptozotocin-induced diabetes

Stress in the kidney is the road to pERdition: is endoplasmic reticulum stress a pathogenic mediator of diabetic nephropathy?

Contact Info

Product

Resources

About