scholarly journals Acrolein cytotoxicity in hepatocytes involves endoplasmic reticulum stress, mitochondrial dysfunction and oxidative stress

2012 ◽  
Vol 265 (1) ◽  
pp. 73-82 ◽  
Author(s):  
Mohammad K. Mohammad ◽  
Diana Avila ◽  
Jingwen Zhang ◽  
Shirish Barve ◽  
Gavin Arteel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mitochondrial Dysfunction ◽  
And Oxidative Stress

scholarly journals Endoplasmic reticulum stress and oxidative stress drive endothelial dysfunction induced by high selenium

2020 ◽  
Author(s):  
Matshediso Zachariah ◽  
Hatem Maamoun ◽  
Larissa Milano ◽  
Margaret P. Rayman ◽  
Lisiane B. Meira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endothelial Dysfunction ◽  
Endoplasmic Reticulum Stress ◽  
High Selenium ◽  
And Oxidative Stress

scholarly journals Research Progress on the Mechanism of Mitochondrial Autophagy in Cerebral Stroke

2021 ◽  
Vol 13 ◽  
Author(s):  
Li Lei ◽  
Shuaifeng Yang ◽  
Xiaoyang Lu ◽  
Yongfa Zhang ◽  
Tao Li
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Ischemic Stroke ◽  
Endoplasmic Reticulum Stress ◽  
Mitochondrial Dysfunction ◽  
Theoretical Basis ◽  
Research Progress ◽  
Cerebral Stroke

Mitochondrial autophagy is an early defense and protection process that selectively clears dysfunctional or excessive mitochondria through a distinctive mechanism to maintain intracellular homeostasis. Mitochondrial dysfunction during cerebral stroke involves metabolic disbalance, oxidative stress, apoptosis, endoplasmic reticulum stress, and abnormal mitochondrial autophagy. This article reviews the research progress on the mechanism of mitochondrial autophagy in ischemic stroke to provide a theoretical basis for further research on mitochondrial autophagy and the treatment of ischemic stroke.

Bilirubin and Epigenetic Modifications in Metabolic and Immunometabolic Disorders

2021 ◽  
Vol 21 ◽  
Author(s):  
Mostafa Moradi Sarabi ◽  
Esmaeel Babaeenezhad ◽  
Maral Amini ◽  
Mozhgan Kaviani ◽  
Fakhraddin Naghibalhossaini
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mitochondrial Dysfunction ◽  
Current Knowledge ◽  
Waste Product ◽  
Epigenetic Modifications ◽  
Mechanisms Of Toxicity ◽  
High Concentrations ◽  
The Brain

: Bilirubin is the main waste product of heme catabolism. At high concentrations, bilirubin may cause toxicity, especially in the brain, kidney, and erythrocytes. Membrane and mitochondrial dysfunction, oxidative stress, apoptosis, necrosis, endoplasmic reticulum stress, excitotoxicity, inflammation, and epigenetic modifications are the main mechanisms of toxicity triggered by bilirubin in susceptible organs. Many studies have shown that there is an interaction between bilirubin and epigenetic modifications in metabolic and immune diseases. In this review, we first outline the toxicity mediated by bilirubin and then summarize the current knowledge linking bilirubin and epigenetic modifications in metabolic and immunometabolic disorders.

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