Senescence marker protein 30 (SMP30) protects against high glucose-induced apoptosis, oxidative stress and inflammatory response in retinal ganglion cells by enhancing Nrf2 activation via regulation of Akt/GSK-3β pathway

2021 ◽  
Vol 101 ◽  
pp. 108238
Author(s):  
Le Zhang ◽  
Tao Zhu ◽  
Fang He ◽  
Xueying Li
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Retinal Ganglion Cells ◽  
High Glucose ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
Marker Protein ◽  
Nrf2 Activation ◽  
Gsk 3Β ◽  
Induced Apoptosis

scholarly journals The novel chalcone analog L2H17 protects retinal ganglion cells from oxidative stress-induced apoptosis

2018 ◽  
Vol 13 (9) ◽  
pp. 1665 ◽  
Author(s):  
Zong-Ming Song ◽  
Xin Zhang ◽  
Lei Wang ◽  
Huai-Cheng Chen ◽  
Xi Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retinal Ganglion ◽  
The Novel ◽  
Induced Apoptosis

scholarly journals Inhibition of TRIM32 Attenuates the Apoptosis, Oxidative Stress and Inflammatory Injury of Podocytes Induced by High Glucose by Affecting the Akt/GSK-3β/Nrf2 Pathway

2021 ◽  
Author(s):  
Zhao Chen ◽  
Lifang Tian ◽  
Li Wang ◽  
Xiaotao Ma ◽  
Fuqian Lei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Inflammatory Response ◽  
High Glucose ◽  
Glycogen Synthase ◽  
Related Factor ◽  
Protective Effects ◽  
Gsk 3Β ◽  
Induced Apoptosis

Abstract Hyperglycemia-induced oxidative stress of podocytes exerts a major role in the pathological process of diabetic nephropathy. Tripartite motif-containing protein 32 (TRIM32) has been reported as a key protein in the modulation of cellular apoptosis and oxidative stress under various pathological processes. However, whether TRIM32 participates in the regulation of high glucose (HG)-induced injury in podocytes has not been investigated. The aims of this work were to assess the possible role of TRIM32 in mediating HG-induced apoptosis, oxidative stress and inflammatory response in podocytes in vitro. Herein, our results showed a marked increase in TRIM32 expression in HG-exposed podocytes. Loss-of-function experiments showed that the knockdown of TRIM32 improved the viability of HG-stimulated podocytes, and suppressed HG-induced apoptosis, oxidative stress and inflammatory response in podocytes. Further investigation revealed that the inhibition of TRIM32 enhanced the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling associated with modulation of the Akt/glycogen synthase kinase-3β (GSK-3β) axis in podocytes following HG exposure. However, the suppression of Akt abrogated the TRIM32-knockdown-mediated activation of Nrf2 in HG-exposed podocytes. In addition, the knockdown of Nrf2 markedly abolished the TRIM32-inhibition-induced protective effects in HG-exposed podocytes. In summary, the results of this work show that the inhibition of TRIM32 protects podocytes from HG-induced injury by potentiating Nrf2 signaling via the modulation of Akt/GSK-3β signaling. This study indicates a potential role of TRIM32 in mediating podocyte injury during the progression of diabetic nephropathy.

Effects of L-Carnitine on High Glucose-Induced Oxidative Stress in Retinal Ganglion Cells

Pharmacology ◽  
2014 ◽  
Vol 94 (3-4) ◽  
pp. 123-130 ◽  
Author(s):  
Yu Cao ◽  
Xin Li ◽  
Ping Shi ◽  
Le-xin Wang ◽  
Zhong-guo Sui
Keyword(s):  
Oxidative Stress ◽  
Retinal Ganglion Cells ◽  
High Glucose ◽  
Ganglion Cells ◽  
Retinal Ganglion
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