Higd1a facilitates exercise-mediated alleviation of fatty liver in diet-induced obese mice

Zhu, Jieying; Chen, Min; Mu, Wang-Jing; Luo, Hong-Yang; Guo, Liang

doi:10.1016/j.metabol.2022.155241

Cited by 24 publications

(19 citation statements)

References 54 publications

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“…Our results indicate that cell hypoxia could be reduced by MSA treatment, and supplemental MSA addition 12 h later could enhance the hypoxia alleviation. Although miR‐3529‐3p was not demonstrated to contribute to hypoxia alleviation, increased miR‐3529‐3p expression was capable of promoting ROS production in lung carcinoma cells because of its ability to disrupt Complex III and IV activities possibly through downregulation of HIGD1A 37,48,49 . Moreover, the ROS elevation induced by miR‐3529‐3p could be enhanced by MSA treatment.…”

Section: Discussionmentioning

confidence: 94%

“…Although miR‐3529‐3p was not demonstrated to contribute to hypoxia alleviation, increased miR‐3529‐3p expression was capable of promoting ROS production in lung carcinoma cells because of its ability to disrupt Complex III and IV activities possibly through downregulation of HIGD1A. 37 , 48 , 49 Moreover, the ROS elevation induced by miR‐3529‐3p could be enhanced by MSA treatment. This is attributed to the fact that MnO 2 can increase the level of ROS in the tumor through fenton reaction in the tumor.…”

Section: Discussionmentioning

confidence: 99%

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Delivery of miR‐3529‐3p using MnO₂‐SiO₂‐APTES nanoparticles combined with phototherapy suppresses lung adenocarcinoma progression by targeting HIGD1A

Zhang

Wang

et al. 2023

Thoracic Cancer

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Background: The present study aimed to investigate the function of miR-3529-3p in lung adenocarcinoma and MnO 2 -SiO 2 -APTES (MSA) as a promising multifunctional delivery agent for lung adenocarcinoma therapy. Methods: Expression levels of miR-3529-3p were evaluated in lung carcinoma cells and tissues by qRT-PCR. The effects of miR-3529-3p on apoptosis, proliferation, metastasis and neovascularization were assessed by CCK-8, FACS, transwell and wound healing assays, tube formation and xenografts experiments. Luciferase reporter assays, western blot, qRT-PCR and mitochondrial complex assay were used to determine the targeting relationship between miR-3529-3p and hypoxia-inducible gene domain family member 1A (HIGD1A). MSA was fabricated using MnO 2 nanoflowers, and its heating curves, temperature curves, IC50, and delivery efficiency were examined. The hypoxia and reactive oxygen species (ROS) production was investigated by nitro reductase probing, DCFH-DA staining and FACS. Results: MiR-3529-3p expression was reduced in lung carcinoma tissues and cells. Transfection of miR-3529-3p could promote apoptosis and suppress cell proliferation, migration and angiogenesis. As a target of miR-3529-3p, HIGD1A expression was downregulated, through which miR-3529-3p could disrupt the activities of complexes III and IV of the respiratory chain. The multifunctional nanoparticle MSA could not only efficiently deliver miR-3529-3p into cells, but also enhance the antitumor function of miR-3529-3p. The underlying mechanism may be that MSA alleviates hypoxia and has synergistic effects in cellular ROS promotion with miR-3529-3p. Conclusions: Our results establish the antioncogenic role of miR-3529-3p, and demonstrate that miR-3529-3p delivered by MSA has enhanced tumor suppressive effects, probably through elevating ROS production and thermogenesis.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Delivery of miR‐3529‐3p using MnO₂‐SiO₂‐APTES nanoparticles combined with phototherapy suppresses lung adenocarcinoma progression by targeting HIGD1A

Zhang

Wang

et al. 2023

Thoracic Cancer

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“…As an important marker of PPARA pathway activation, ACADM regulates fatty acid oxidation and export in hepatocytes in NAFLD. 30 As the main intervention target of statins, HMGCR has been widely verified in the clinical prevention and treatment of hyperlipidaemia and atherosclerosis. HMCGR remains the central gene of NAFLD, and its high expression is an important factor in the accumulation of fatty acids in the liver.…”

Section: Discussionmentioning

confidence: 99%

A UPLC-Q-TOF/MS and network pharmacology method to explore the mechanism of Anhua fuzhuan tea intervention in nonalcoholic fatty liver disease

Tian

Tang

et al. 2023

Food Funct.

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“…In general, animal fats are rich in saturated fatty acids palmitate and stearate, which are directly toxic to cells ( Packard et al, 2020 ), while monounsaturated fatty acids could prevent saturated fatty acid-induced cytotoxicity ( Urso and Zhou, 2021 ). Saturated fatty acids could induce hepatic endoplasmic reticulum stress and promote inflammasome activation, which could also activate amino-terminal kinase (JNK) and mitochondrial death pathways to induce hepatocyte apoptosis ( Luci et al, 2020 ; Zhu et al, 2022 ). Increased hepatocyte free fatty acids could form lipotoxic intermediates in the liver, such as ceramides, diacylglycerols, lysophosphatidylcholines, oxidized fatty acids, and cholesterol metabolites, which act like ROS ( Sowton et al, 2020 ).…”

Section: Intrahepatic Factors In Nashmentioning

confidence: 99%

Recent evaluation about inflammatory mechanisms in nonalcoholic fatty liver disease

Long

Huang

2023

Front. Pharmacol.

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Non-alcoholic fatty liver disease (NAFLD) is common chronic metabolic liver disorder which is associated with fat accumulation in the liver. It causes a wide range of pathological effects such as insulin resistance, obesity, hypertension, diabetes, non-alcoholic steatohepatitis (NASH) and cirrhosis, cardiovascular diseases. The molecular mechanisms that cause the initiation and progression of NAFLD remain fully unclear. Inflammation is regarded as a significant mechanism which could result in cell death and tissue injury. Accumulation of leukocytes and hepatic inflammation are important contributors in NAFLD. Excessive inflammatory response can deteriorate the tissue injury in NAFLD. Thus, inhibition of inflammation improves NAFLD by reducing intrahepatic fat content, increasing β-oxidation of fatty acids, inducing hepato-protective autophagy, overexpressing peroxisome proliferator-activated receptor- γ (PPAR-γ), as well as attenuating hepatocyte apoptosis and increasing insulin sensitivity. Therefore, understanding the molecules and signaling pathways suggests us valuable information about NAFLD progression. This review aimed to evaluate the inflammation in NAFLD and the molecular mechanism on NAFLD.

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Higd1a facilitates exercise-mediated alleviation of fatty liver in diet-induced obese mice

Cited by 24 publications

References 54 publications

Delivery of miR‐3529‐3p using MnO₂‐SiO₂‐APTES nanoparticles combined with phototherapy suppresses lung adenocarcinoma progression by targeting HIGD1A

Delivery of miR‐3529‐3p using MnO₂‐SiO₂‐APTES nanoparticles combined with phototherapy suppresses lung adenocarcinoma progression by targeting HIGD1A

A UPLC-Q-TOF/MS and network pharmacology method to explore the mechanism of Anhua fuzhuan tea intervention in nonalcoholic fatty liver disease

Recent evaluation about inflammatory mechanisms in nonalcoholic fatty liver disease

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Higd1a facilitates exercise-mediated alleviation of fatty liver in diet-induced obese mice

Cited by 24 publications

References 54 publications

Delivery of miR‐3529‐3p using MnO2‐SiO2‐APTES nanoparticles combined with phototherapy suppresses lung adenocarcinoma progression by targeting HIGD1A

Delivery of miR‐3529‐3p using MnO2‐SiO2‐APTES nanoparticles combined with phototherapy suppresses lung adenocarcinoma progression by targeting HIGD1A

A UPLC-Q-TOF/MS and network pharmacology method to explore the mechanism of Anhua fuzhuan tea intervention in nonalcoholic fatty liver disease

Recent evaluation about inflammatory mechanisms in nonalcoholic fatty liver disease

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Delivery of miR‐3529‐3p using MnO₂‐SiO₂‐APTES nanoparticles combined with phototherapy suppresses lung adenocarcinoma progression by targeting HIGD1A

Delivery of miR‐3529‐3p using MnO₂‐SiO₂‐APTES nanoparticles combined with phototherapy suppresses lung adenocarcinoma progression by targeting HIGD1A