Overexpression of miR-29ab1 Cluster Results in Excessive Muscle Growth in 1-Month-old Mice by Inhibiting <i>Mstn</i>

Liu, Chuncheng; Cao, Yuxin; Li, Lei; Wang, Yiting; Meng, Qingyong

doi:10.1089/dna.2022.0247

DNA and Cell Biology

2023

DOI: 10.1089/dna.2022.0247

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Overexpression of miR-29ab1 Cluster Results in Excessive Muscle Growth in 1-Month-old Mice by Inhibiting Mstn

Chuncheng Liu

Yuxin Cao

Lei Li

et al.

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Cited by 2 publications

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Transcriptome Analysis of the Effect of Nickel on Lipid Metabolism in Mouse Kidney

Zhang,

Gao,

et al. 2024

Biology

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Although the human body needs nickel as a trace element, too much nickel exposure can be hazardous. The effects of nickel on cells include inducing oxidative stress, interfering with DNA damage repair, and altering epigenetic modifications. Glucose metabolism and lipid metabolism are closely related to oxidative stress; however, their role in nickel-induced damage needs further study. In Institute of Cancer Research (ICR) mice, our findings indicated that nickel stress increased the levels of blood lipid indicators (triglycerides, high-density lipoprotein, and cholesterol) by about 50%, blood glucose by more than two-fold, and glycated serum protein by nearly 20%. At the same time, nickel stress increased oxidative stress (malondialdehyde) and inflammation (Interleukin 6) by about 30% in the kidney. Based on next-generation sequencing technology, we detected and analyzed differentially expressed genes in the kidney caused by nickel stress. Bioinformatics analysis and experimental verification showed that nickel inhibited the expression of genes related to lipid metabolism and the AMPK and PPAR signaling pathways. The finding that nickel induces kidney injury and inhibits key genes involved in lipid metabolism and the AMPK and PPAR signaling pathways provides a theoretical basis for a deeper understanding of the mechanism of nickel-induced kidney injury.

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Transcriptome Analysis of the Effect of Nickel on Lipid Metabolism in Mouse Kidney

Zhang,

Gao,

et al. 2024

Biology

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マイクロrnaによる骨格筋量の調節

Shin,

Akimoto

2023

Tairyoku Kagaku

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Skeletal muscle is a vital tissue not only for maintaining posture and body movements but also for energy metabolism in human body. Skeletal muscle is highly plastic in response to various stimuli, resistance exercise or anabolic hormones can increase muscle mass, which is termed "muscle hypertrophy". Contrary, immobility, aging and severe illness can reduce muscle mass, which is termed "muscle atrophy". Loss of skeletal muscle mass is associated with loss of independent living, the morbidity of a variety of diseases and mortality throughout life. Therefore, understanding mechanisms that regulate skeletal muscle mass is essential for improving the quality of life. Recent studies reported microRNAs (miRNAs), which is a class of non-coding RNAs, play a crucial role in the regulation of muscle mass. This review provides a current understanding of the function of miRNAs in regulation of skeletal muscle mass.

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Overexpression of miR-29ab1 Cluster Results in Excessive Muscle Growth in 1-Month-old Mice by Inhibiting Mstn

Cited by 2 publications

References 35 publications

Transcriptome Analysis of the Effect of Nickel on Lipid Metabolism in Mouse Kidney

Transcriptome Analysis of the Effect of Nickel on Lipid Metabolism in Mouse Kidney

マイクロrnaによる骨格筋量の調節

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