Zanthoxylum armatum DC. extract induces liver injury via autophagy suppression and oxidative damage by activation of mTOR/ULK1 pathway

Huang, Yan; Jiang, Jialuo; Wang, Wenlin; Guo, Jiafu; Yang, Nannan; Zhang, Jian; Liu, Qiuyan; Chen, Yan; Hu, Tingting; Rao, Chaolong

doi:10.1016/j.toxicon.2022.08.008

Cited by 8 publications

(2 citation statements)

References 55 publications

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“…Autophagy can play a regulatory role in maintaining cell homeostasis. Studies have found that the administration of exogenous chemicals to hepatocytes can inhibit the occurrence of autophagy and then induce cell death, which can be inhibited by rapamycin (autophagy inducer) [ 58 ]. It is widely thought that a mutual regulatory relationship exists between ERS-induced autophagy and apoptosis.…”

Section: Cell Death Mediated By Ers and Uprmentioning

confidence: 99%

Endoplasmic reticulum stress-mediated cell death in liver injury

et al. 2022

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The endoplasmic reticulum is an important intracellular organelle that plays an important role in maintaining cellular homeostasis. Endoplasmic reticulum stress (ERS) and unfolded protein response (UPR) are induced when the body is exposed to adverse external stimuli. It has been established that ERS can induce different cell death modes, including autophagy, apoptosis, ferroptosis, and pyroptosis, through three major transmembrane receptors on the ER membrane, including inositol requirement enzyme 1α, protein kinase-like endoplasmic reticulum kinase and activating transcription factor 6. These different modes of cell death play an important role in the occurrence and development of various diseases, such as neurodegenerative diseases, inflammation, metabolic diseases, and liver injury. As the largest metabolic organ, the liver is rich in enzymes, carries out different functions such as metabolism and secretion, and is the body’s main site of protein synthesis. Accordingly, a well-developed endoplasmic reticulum system is present in hepatocytes to help the liver perform its physiological functions. Current evidence suggests that ERS is closely related to different stages of liver injury, and the death of hepatocytes caused by ERS may be key in liver injury. In addition, an increasing body of evidence suggests that modulating ERS has great potential for treating the liver injury. This article provided a comprehensive overview of the relationship between ERS and four types of cell death. Moreover, we discussed the mechanism of ERS and UPR in different liver injuries and their potential therapeutic strategies.

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Section: Cell Death Mediated By Ers and Uprmentioning

confidence: 99%

Endoplasmic reticulum stress-mediated cell death in liver injury

et al. 2022

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“…They observed that MZADC inhibited the lipidation of LC3-I and degradation of P62. MZADC-induced autophagy reduction and oxidative damage were significantly recovered in BRL 3A cells when pretreated with RAPA [ 143 ].…”

Section: Potential Therapeutic Effects Of Natural Products On Liver D...mentioning

confidence: 99%

Natural-Product-Mediated Autophagy in the Treatment of Various Liver Diseases

Fan

Wang

et al. 2022

IJMS

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Autophagy is essential for the maintenance of hepatic homeostasis, and autophagic malfunction has been linked to the pathogenesis of substantial liver diseases. As a popular source of drug discovery, natural products have been used for centuries to effectively prevent the progression of various liver diseases. Emerging evidence has suggested that autophagy regulation is a critical mechanism underlying the therapeutic effects of these natural products. In this review, relevant studies are retrieved from scientific databases published between 2011 and 2022, and a novel scoring system was established to critically evaluate the completeness and scientific significance of the reviewed literature. We observed that numerous natural products were suggested to regulate autophagic flux. Depending on the therapeutic or pathogenic role autophagy plays in different liver diseases, autophagy-regulative natural products exhibit different therapeutic effects. According to our novel scoring system, in a considerable amount of the involved studies, convincing and reasonable evidence to elucidate the regulatory effects and underlying mechanisms of natural-product-mediated autophagy regulation was missing and needed further illustration. We highlight that autophagy-regulative natural products are valuable drug candidates with promising prospects for the treatment of liver diseases and deserve more attention in the future.

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