Deficiency of apoptosis-stimulating protein 2 of p53 protects mice from acute hepatic injury induced by CCl4 via autophagy

Xu, Ping; Yao, Jia; Ji, Jing; Shi, Hang; Jiao, Yan; Hao, Shasha; Chen, Dexi

doi:10.1016/j.toxlet.2019.09.006

Cited by 12 publications

(18 citation statements)

References 30 publications

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“…Although knockout of Ulk1/2 did not alter the autophagic activity of hepatocytes in mice upon overnight fasting, these mice showed strong resistance to APAP‐induced ALI via activation of JNK signalling both in vivo and in vitro 73 . Deletion of apoptosis‐stimulating protein 2 of p53 (ASPP2) in mice protected them from CCl 4 ‐induced ALI via activation of autophagy and reduction of cellular inflammation and apoptosis, as shown by decreased ALT and AST levels and reduced hepatic tissue haemorrhage and necrosis 74 . According to these studies, we predict that genetic modifications will repair liver injury by regulating autophagy.…”

Section: Autophagy and Chemically Induced Ali In Animal Modelsmentioning

confidence: 92%

“…33 Another study indicated that the caspase-9 inhibitor z-LEHD-FMK aggravated CCl 4 -induced ALI in hepatic tissue haemorrhage and necrosis. 74 According to these studies, we predict that genetic modifications will repair liver injury by regulating autophagy.…”

Section: Modulation Of Autophagy Reduces CCL 4induced Alimentioning

confidence: 99%

“…66 Pretreatment with genipin has been proven to induce the conversion of LC3 and inhibit p62 accumulation in vivo, subsequently attenuating hepatic tissue haemorrhage and necrosis. 74 According to these studies, we predict that genetic modifications will repair liver injury by regulating autophagy.…”

Section: Modulation Of Autophagy Reduces CCL 4induced Alimentioning

confidence: 99%

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Autophagy regulation is an effective strategy to improve the prognosis of chemically induced acute liver injury based on experimental studies

Zhao

Shen

et al. 2020

J Cellular Molecular Medi

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Acute liver injury (ALI) induced by chemicals in current experimental studies is characterized by inflammation, oxidative stress and necrosis, which can greatly influence the long‐term outcome and lead to liver failure. In liver cells, different autophagy forms envelop cytoplasm components, including proteins, endoplasmic reticulum (ER), mitochondria and lipids, and they effectively participate in breaking down the cargo enclosed inside lysosomes to replenish cellular energy and contents. In general, autophagy serves as a cell survival mechanism in stressful microenvironments, but it also serves as a destructive mechanism that results in cell death in vitro and in vivo. In experimental animals, multiple chemicals are used to mimic ALI in patients to clarify the potential pathological mechanisms and develop effective strategies in the clinic. In this review, we summarize related publications about autophagy modulation to attenuate chemically induced ALI in vitro and in vivo. We also analysed the underlying mechanisms of autophagy regulators and genetic modifications to clarify how to control autophagy to protect against chemically induced ALI in animal models. We anticipate that selectively controlling the dual effects of hepatic autophagy will help to protect against ALI in various animals, but the detailed mechanisms and effects should be determined further in future studies. In this way, we are more confident that modulating autophagy in liver regeneration can improve the prognosis of ALI.

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Section: Autophagy and Chemically Induced Ali In Animal Modelsmentioning

confidence: 92%

Section: Modulation Of Autophagy Reduces CCL 4induced Alimentioning

confidence: 99%

See 1 more Smart Citation

Autophagy regulation is an effective strategy to improve the prognosis of chemically induced acute liver injury based on experimental studies

Zhao

Shen

et al. 2020

J Cellular Molecular Medi

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“…To determine whether ASPP1 is involved in liver injury, we first detected its expression alterations in WT mice treated with CCl4 to induce hepatic injury [12]. To this end, the animals were administered with 5% CCl4 (1:19 v/v in olive oil) at a dose of 2µL/ g body weight by intraperitoneal injection and sacrificed after 24 hrs.…”

Section: Expression Of Aspp1 and Alt/ast In Wild Type Mice Treated With Ccl4mentioning

confidence: 99%

“…For example, it regulates the pathogenesis and progression of acute lymphoblastic leukemia, and its methylation helps acute lymphoblastic leukemia cell (ALL) to escape apoptosis [11]. It was reported that ASSPP2 knockout protected liver from inflammation and apoptosis induced by CCl4 via activating autophagy [12].…”

Section: Introductionmentioning

confidence: 99%

Ablation of apoptosis-stimulating of p53 protein 1 protects mice from acute hepatic injury and dysfunction via NF-κB pathway in CCl4-induced hepatotoxicity

Daba

Huang

Yagudin

et al. 2021

Frigid Zone Medicine

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Acute liver injury (ALI) is characterized by apoptosis, inflammation, and oxidative stress, and pathogenic mechanism of ALI is poorly understood. Apoptosis-stimulating of p53 protein 1 (ASPP1) is involved in environmental responses, tumor growth, and NF-KB activity, which is of critical importance to ALI. However, the role of ASPP1 in ALI remains largely unexplored. The current study aimed to determine the role of ASPP1 in ALI induced by CCl4 and the underlying mechanism. ASPP1 expression was detected in wild type (WT) mice with ALI induced by CCl4. The function of ASPP1 in ALI induced by CCl4 was investigated using conventional knockout ASPP1 mice. ASPP1 expression significantly increased in ALI mice at 24 hours after CCl4 injection. Deletion of ASSP1 ameliorated apoptosis, inflammation, and necrosis in ALI relative to WT mice. In addition, deficiency of ASPP1 improved liver flood flow as well as ALT and AST levels. The levels of phosphorylated p65 and phosphorylated IκBα were lower in ASPP1-/- mice than in WT mice with ALI. These results implicate that deletion of ASPP1 may act via inhibition of the NF-κB pathway and protect mice from ALI, which may be a new potential therapeutic target for the treatment of ALI.

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ASPP2 reduction attenuates HBV induced chronic liver damage: A hybrid mouse model study

Wang

Che

Wang

et al. 2022

Biochemical and Biophysical Research Communications

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Deficiency of apoptosis-stimulating protein 2 of p53 protects mice from acute hepatic injury induced by CCl4 via autophagy

Cited by 12 publications

References 30 publications

Autophagy regulation is an effective strategy to improve the prognosis of chemically induced acute liver injury based on experimental studies

Autophagy regulation is an effective strategy to improve the prognosis of chemically induced acute liver injury based on experimental studies

Ablation of apoptosis-stimulating of p53 protein 1 protects mice from acute hepatic injury and dysfunction via NF-κB pathway in CCl4-induced hepatotoxicity

ASPP2 reduction attenuates HBV induced chronic liver damage: A hybrid mouse model study

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