Nuclear miR-150 enhances hepatic lipid accumulation by targeting RNA transcripts overlapping the PLIN2 promoter

Luo, Jiao; Ji, Yanan; Chen, Ningning; Song, Ge; Zhou, Shuyue; Niu, Xuan; Yu, Dianke

doi:10.1016/j.isci.2023.107837

iScience

2023

DOI: 10.1016/j.isci.2023.107837

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Nuclear miR-150 enhances hepatic lipid accumulation by targeting RNA transcripts overlapping the PLIN2 promoter

Jiao Luo,

Yanan Ji,

Ningning Chen

et al.

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Cited by 3 publications

References 49 publications

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Luo,

Zhou

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Biochemical Pharmacology

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Lysine β-hydroxybutyrylation promotes lipid accumulation in alcoholic liver disease

Chen,

Luo,

Zhou

et al. 2023

Biochemical Pharmacology

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piR-27222 mediates PM2.5-induced lung cancer by resisting cell PANoptosis through the WTAP/m6A axis

Ma,

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Wang

et al. 2024

Environment International

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Hepatic‐specific Pgc‐1α ablation drives fibrosis in a MASH model

Arconzo,

Piccinin,

Pasculli

et al. 2024

Liver International

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Background & AimsMetabolic dysfunction‐associated steatohepatitis (MASH) is a growing cause of chronic liver disease, characterized by fat accumulation, inflammation and fibrosis, which development depends on mitochondrial dysfunction and oxidative stress. Highly expressed in the liver during fasting, peroxisome proliferator‐activated receptor‐γ coactivator‐1α (PGC‐1α) regulates mitochondrial and oxidative metabolism. Given the relevant role of mitochondrial function in MASH, we investigated the relationship between PGC‐1α and steatohepatitis.MethodsWe measured the hepatic expression of Pgc‐1α in both MASH patients and wild‐type mice fed a western diet (WD) inducing steatosis and fibrosis. We then generated a pure C57BL6/J strain loss of function mouse model in which Pgc‐1α is selectively deleted in the liver and we fed these mice with a WD supplemented with sugar water that accurately mimics human MASH.ResultsWe observed that the hepatic expression of Pgc‐1α is strongly reduced in MASH, in both humans and mice. Moreover, the hepatic ablation of Pgc‐1α promotes a considerable reduction of the hepatic mitochondrial respiratory capacity, setting up a bioenergetic harmful environment for liver diseases. Indeed, the lack of Pgc‐1α decreases mitochondrial function and increases inflammation, fibrosis and oxidative stress in the scenario of MASH. Intriguingly, this profibrotic phenotype is not linked with obesity, insulin resistance and lipid disbalance.ConclusionsIn a MASH model the hepatic ablation of Pgc‐1α drives fibrosis independently from lipid and glucose metabolism. These results add a novel mechanistic piece to the puzzle of the specific and crucial role of mitochondrial function in MASH development.

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Nuclear miR-150 enhances hepatic lipid accumulation by targeting RNA transcripts overlapping the PLIN2 promoter

Cited by 3 publications

References 49 publications

Lysine β-hydroxybutyrylation promotes lipid accumulation in alcoholic liver disease

Lysine β-hydroxybutyrylation promotes lipid accumulation in alcoholic liver disease

piR-27222 mediates PM2.5-induced lung cancer by resisting cell PANoptosis through the WTAP/m6A axis

Hepatic‐specific Pgc‐1α ablation drives fibrosis in a MASH model

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