- Obesity and Metabolism
- Cellular and Intercellular Homeostasis in Adipose Tissue with Mitochondria-Specific Stress
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Min Jeong Choi, Saet-Byel Jung, Joon Young Chang, Minho Shong
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Endocrinol Metab. 2021;36(1):1-11. Published online February 24, 2021
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DOI: https://doi.org/10.3803/EnM.2021.956
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- Paracrine interactions are imperative for the maintenance of adipose tissue intercellular homeostasis, and intracellular organelle dysfunction results in local and systemic alterations in metabolic homeostasis. It is currently accepted that mitochondrial proteotoxic stress activates the mitochondrial unfolded protein response (UPRmt) in vitro and in vivo. The induction of mitochondrial chaperones and proteases during the UPRmt is a key cell-autonomous mechanism of mitochondrial quality control. The UPRmt also affects systemic metabolism through the secretion of cell non-autonomous peptides and cytokines (hereafter, metabokines). Mitochondrial function in adipose tissue plays a pivotal role in whole-body metabolism and human diseases. Despite continuing interest in the role of the UPRmt and quality control pathways of mitochondria in energy metabolism, studies on the roles of the UPRmt and metabokines in white adipose tissue are relatively sparse. Here, we describe the role of the UPRmt in adipose tissue, including adipocytes and resident macrophages, and the interactive roles of cell non-autonomous metabokines, particularly growth differentiation factor 15, in local adipose cellular homeostasis and systemic energy metabolism.
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Citations
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- Imeglimin modulates mitochondria biology and facilitates mitokine secretion in 3T3-L1 adipocytes
Nobuhiko Takahashi, Atsushi P. Kimura, Takayuki Yoshizaki, Kazumasa Ohmura Life Sciences.2024; 349: 122735. CrossRef - Mitochondrial stress-induced GFRAL signaling controls diurnal food intake and anxiety-like behavior
Carla Igual Gil, Bethany M Coull, Wenke Jonas, Rachel N Lippert, Susanne Klaus, Mario Ost Life Science Alliance.2022; 5(11): e202201495. CrossRef - Stress-induced FGF21 and GDF15 in obesity and obesity resistance
Susanne Keipert, Mario Ost Trends in Endocrinology & Metabolism.2021; 32(11): 904. CrossRef
- Thyroid
- Mitochondrial Energy Metabolism and Thyroid Cancers
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Junguee Lee, Joon Young Chang, Yea Eun Kang, Shinae Yi, Min Hee Lee, Kyong Hye Joung, Kun Soon Kim, Minho Shong
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Endocrinol Metab. 2015;30(2):117-123. Published online June 30, 2015
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DOI: https://doi.org/10.3803/EnM.2015.30.2.117
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Primary thyroid cancers including papillary, follicular, poorly differentiated, and anaplastic carcinomas show substantial differences in biological and clinical behaviors. Even in the same pathological type, there is wide variability in the clinical course of disease progression. The molecular carcinogenesis of thyroid cancer has advanced tremendously in the last decade. However, specific inhibition of oncogenic pathways did not provide a significant survival benefit in advanced progressive thyroid cancer that is resistant to radioactive iodine therapy. Accumulating evidence clearly shows that cellular energy metabolism, which is controlled by oncogenes and other tumor-related factors, is a critical factor determining the clinical phenotypes of cancer. However, the role and nature of energy metabolism in thyroid cancer remain unclear. In this article, we discuss the role of cellular energy metabolism, particularly mitochondrial energy metabolism, in thyroid cancer. Determining the molecular nature of metabolic remodeling in thyroid cancer may provide new biomarkers and therapeutic targets that may be useful in the management of refractory thyroid cancers.
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Citations
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