ABSTRACT
Adipose tissue is a major energy storage and endocrine organ. Adipogenesis is a complex process of cell differentiation, which is regulated by nutrient levels, hormones and metabolites, etc. The mammalian target of rapamycin (mTOR) complex includes two protein complexes, mammalian target of rapamycin complex 1 (mTORC1) and mTORC2. The lipid kinase-like domain contained in the mTOR complex lays the foundation for the mTOR pathway to regulate adipogenesis. Research on some components of mTORC1 and mTORC2 has verified the roles of mTOR in the regulation of adipogenesis. Based on previous studies, we reviewed the research of miR-199a-3p, miR-103, miR-188, Src-associated substrate in mitosis of 68 kD (Sam68), endostatin and other substances in the regulation of adipogenesis through mTORC1 and mTORC2. At the same time, we had further constructed the adipogenesis network regulated by mTOR signaling pathway, including insulin/IGF pathway, PI3K-AKT pathway, amino acid pathway, AMPK pathway, cAMP pathway, cGMP pathway, NOTCH pathway, and the modulation of bta-miR-150, 4-O-methylasochlorin and a variety of proteins. This article mainly reviewed the characteristics of mTOR complex and the latest research progress in the regulation of adipogenesis by mTOR pathway. It was pointed out that mTORC2 can regulate lipid uptake, lipolysis and regulate the function of mTORC1. However, there are fewer studies on mTORC2 compared to mTORC1, so further researches on adipogenesis and lipid metabolism may be more focused on mTORC2.
ABSTRACT
Skeletal muscle is an important tissue of human and livestock. The study of the muscle development is of great significance for treating muscle diseases and improving livestock meat quality. The process of muscle development is controlled by several myogenic transcription factors and signaling pathways. In addition, recent findings established that several noncoding RNAs play a critical role in the regulation of muscle development such as long non-coding RNA (lncRNA), microRNA (miRNA) and circu- lar RNA (circRNA), etc. The detailed mechanism of muscle development is not well understood. Transfer RNAs (tRNAs) are fundamental components in the translation machinery as an adaptor molecule, and tRNA pool could be differentially exploited to modulate expression of mRNAs. In addition, tRNA can be cleaved into tRNA-derived fragments (tRFs) by a variety of ribonucleases (RNases) upon various stress conditions. Unlike the post-transcriptional regulation of lncRNA and miRNA on muscle development, tRNA has been implicated in various aspects of muscle development. Mitochondria play a central role in a plethora of processes related to the maintenance of muscle cellular homeostasis and genomic integrity. Mitochondrial tRNA(mt-tRNA) gene mutations lead to multiple myopathy because human mitochondrial genome is extremely small. The regulation of tRF is similar to miRNAs in regards to the related physiological processes, but are more conservative than miRNA. It is generally believed that tRF has strong tissue specificity, disease specificity and temporal specificity. Some skeletal muscle-specific tRFs could act posttranscriptionally via RNAi or targeting related genes. However, the tRF-sequencing analysis and functional mechanism of tRF are rarely studied in skeletal muscles. The myopathy caused by mitochondrial tRNA gene mutations are particularly complex, which are one of the challenges to diagnose, treat, or prevent diseases. Compared with other noncoding RNAs, the structural complexity of tRF also brings great challenges to data mining and analysis. In this review, we summarize the formation and function of tRNA and tRF especially in muscle development, which will deepen our understandings of related myopathy, and provide new ideas and directions for the investigation of skeletal muscle.