نتایج جستجو برای: liver injury autophagy

تعداد نتایج: 619356  

Journal: :International journal of molecular medicine 2014
Yun Wang Xuanxuan Xiong Hao Guo Mingbo Wu Xiangcheng Li Yuanchao Hu Guangwei Xie Jian Shen Qingzhong Tian

There is growing evidence indicating that autophagy plays a protective role in liver ischemia/reperfusion (IR) injury. Heme oxygenase-1 (HO-1) can also prevent liver IR injury by limiting inflammation and inducing an anti-apoptotic response. Autophagy also plays a crucial role in liver IR injury. The aim of the present study was to investigate the role of HO-1 in liver IR injury and the associa...

2013
Hong-Min Ni Jessica A Williams Hartmut Jaeschke Wen-Xing Ding

Acetaminophen (APAP) overdose is the most frequent cause of acute liver failure in the US and many western countries. It is well known that APAP induces mitochondrial damage to trigger centrilobular necrosis. Emerging evidence suggests that autophagic removal of damaged mitochondria may protect against APAP-induced liver injury. Electron and confocal microscopy analysis of liver tissues reveale...

Journal: :Cell 2007
Masaaki Komatsu Satoshi Waguri Masato Koike Yu-shin Sou Takashi Ueno Taichi Hara Noboru Mizushima Jun-ichi Iwata Junji Ezaki Shigeo Murata Jun Hamazaki Yasumasa Nishito Shun-ichiro Iemura Tohru Natsume Toru Yanagawa Junya Uwayama Eiji Warabi Hiroshi Yoshida Tetsuro Ishii Akira Kobayashi Masayuki Yamamoto Zhenyu Yue Yasuo Uchiyama Eiki Kominami Keiji Tanaka

Inactivation of constitutive autophagy results in formation of cytoplasmic protein inclusions and leads to liver injury and neurodegeneration, but the details of abnormalities related to impaired autophagy are largely unknown. Here we used mouse genetic analyses to define the roles of autophagy in the aforementioned events. We report that the ubiquitin- and LC3-binding protein "p62" regulates t...

Journal: :Molecular and Cellular Oncology 2021

Selective autophagy contributes to the degradation of condensates, such as sequestosome 1-bodies, also called p62/SQSTM1-bodies. We showed that endogenous p62 forms gel-like structures, which serve platforms for autophagosome formation and nuclear factor erythroid 2-related 2 (NRF2) activation. Further, p62-mediated NRF2 activation is not cytotoxic, but combination with impaired bulk selective ...

2014
Yuan Li Shaogui Wang Hong-Min Ni Heqing Huang Wen-Xing Ding

Autophagy is a genetically programmed, evolutionarily conserved intracellular degradation pathway involved in the trafficking of long-lived proteins and cellular organelles to the lysosome for degradation to maintain cellular homeostasis. Alcohol consumption leads to injury in various tissues and organs including liver, pancreas, heart, brain, and muscle. Emerging evidence suggests that autopha...

Introduction: In many cultures fasting is recommended as a way to protect and promote health. However, there are few studies on the effects of fasting on organ function and resistance to toxic agents such as drugs. This study was conducted to investigate the effect of short-term periodic fasting on the acetaminophen hepatotoxic effects in mice. Methods: In this...

2016
Meihua Piao Ya Liu Ting Yu Ying Lu

This article explored the protective effects of zinc supplementation on diabetic liver injury and studied the underlying mechanisms that zinc supplementation reduced ER stress and autophagy in diabetic liver. Type 2 diabetes mellitus-like Wistar rat models were intragastrically administrated with ZnSO4 15 mg/kg daily for 53 days. Liver changes were examined by biochemical assay of serum, histop...

Journal: :American journal of physiology. Gastrointestinal and liver physiology 2016
Youcai Tang Peter Fickert Michael Trauner Nancy Marcus Keith Blomenkamp Jeffrey Teckman

The bile acid nor-ursodeoxycholic acid (norUDCA) has many biological actions, including antiapoptotic effects. Homozygous PIZZ α-1-antitrypsin (A1AT)-deficient humans are known to be at risk for liver disease, cirrhosis, and liver cancer as a result of the accumulation of the toxic, A1AT mutant Z protein within hepatocytes. This accumulation triggers cell death in the hepatocytes with the large...

Journal: :Biocell 2021

Wilson disease (WD), known as hepatolenticular degeneration (HLD), is a treatable autosomal recessive disorder of copper metabolism. Because deposits in the liver first, not only original defective organ but also most affected organ. The injury one main causes death throughout course disease. Therefore, treatment task WD treatment, which great significance to improve prognosis patients. Autopha...

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