<i>In vivo</i> recognition of bioactive substances of <i>Polygonum multiflorum</i> for regulating mitochondria against metabolic dysfunction-associated fatty liver disease

Yu, Liping; Li, Yanjuan; Wang, Tao; Tao, Yu-Xuan; Zhang, Mei; Gu, Wen; Yu, Jie; Yang, Xiao‐Ke

doi:10.3748/wjg.v29.i1.171

Cited by 3 publications

(1 citation statement)

References 28 publications

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“…For the paper “ In vivo recognition of bioactive substances of Polygonum multiflorum for protecting mitochondria against metabolic dysfunction-associated fatty liver disease”, the title is not precise. Possibly, it would be better to replace “…for regulating mitochondria...” with “…for protecting mitochondria…” since you cannot regulate against something[ 3 ].…”

Section: Hot Articles and Insufficient Articlesmentioning

confidence: 99%

Editor-in-Chief articles of choice and comments at the year-end of 2023

Tarnawski

2024

World J Gastroenterol

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As the Editor-in-Chief, every week prior to a new issue’s online publication, I perform a careful review of all encompassed articles, including the title, clinical and/or research importance, originality, novelty, and ratings by the peer reviewers. Based on this review, I select the papers of choice and suggest pertinent changes (e.g. , in the title) to the Company Editors responsible for publication. This process, while time-consuming, is very important for assuring the quality of publications and highlighting important articles that Readers may revisit.

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Section: Hot Articles and Insufficient Articlesmentioning

confidence: 99%

Editor-in-Chief articles of choice and comments at the year-end of 2023

Tarnawski

2024

World J Gastroenterol

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New insights into the role of mitochondrial dynamics in oxidative stress-induced diseases

Chen,

Li,

Shi

et al. 2024

Biomedicine & Pharmacotherapy

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Pharmacological Activation of AMPK Prevents Drp1-mediated Mitochondrial Fission and Alleviates Hepatic Steatosis In vitro

Du,

Wang,

Xiao

et al. 2024

CMM

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Background: The incidence of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide. Adenosine monophosphate-activated protein kinase (AMPK) activation is beneficial for NAFLD treatment. Recent studies show the excessive fission of mitochondria during NAFLD progression, so targeting mitochondria dynamics may be a possible target for NAFLD. Still, little is known about whether AMPK regulates mitochondrial dynamics in hepar. Objective: This study investigated whether AMPK activation alleviates hepatic steatosis by regulating mitochondrial dynamics mediated by GTPase dynamin-related protein 1 (Drp1). Methods: Human hepatocyte line L-02 cells were cultured and subjected to palmitic acid (PA) treatment for 24 h to establish a hepatic steatosis model in vitro, which was pre-treated with different tool drugs. Hepatocyte function, hepatocyte lipid content, mitochondrial reactive oxygen species (ROS) production, and mitochondrial membrane potential (MMP) were examined. The expression levels of genes and proteins associated with mitochondrial dynamics were assessed using reverse transcription-quantitative PCR and western blotting. Results: The results indicated that 5-Aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR), an AMPK activator, improved hepatocyte function, as demonstrated by decreased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity (P＜0.05 or P＜0.01). In addition, AICAR decreased total cholesterol (TC) and triglyceride (TG) content and lipid deposition in hepatocytes (P＜0.01); decreased ROS production; improved MMP (P＜0.01); reduced fission-1 (Fis1) and mitochondrial fission factor (Mff) mRNA expression; and downregulated p-Drp1 (Ser 616) protein expression. In contrast, AICAR increased mitochondrial fusion factor mitofusin-1 (Mfn1) and mitofusin-2 (Mfn2) mRNA expression and upregulated p-Drp1 (Ser 637) protein expression. Mdivi-1, a Drp-1 inhibitor, was used to confirm whether mitochondrial dynamics regulated by Drp1-mediated the role of AICAR. Similar to AICAR, Mdivi-1 improved hepatocyte function and MMP significantly, decreased ROS production and lipid deposition, downregulated Fis1 and Mff mRNA expression, downregulated p-Drp1 (Ser 616) protein expression, and enhanced Mfn1 and Mfn2 mRNA and p-Drp1 (Ser 637) protein expression. However, Compound C, an AMPKspecific inhibitor, had less impact on the protective effect of Mdivi-1. Conclusion: The results demonstrated that AMPK activation has a protective effect on hepatic steatosis in vitro, largely dependent on the inhibition of Drp1-mediated mitochondrial fission.

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In vivo recognition of bioactive substances of Polygonum multiflorum for regulating mitochondria against metabolic dysfunction-associated fatty liver disease

Cited by 3 publications

References 28 publications

Editor-in-Chief articles of choice and comments at the year-end of 2023

Editor-in-Chief articles of choice and comments at the year-end of 2023

New insights into the role of mitochondrial dynamics in oxidative stress-induced diseases

Pharmacological Activation of AMPK Prevents Drp1-mediated Mitochondrial Fission and Alleviates Hepatic Steatosis In vitro

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