Specific and efficient gene knockout and overexpression in mouse interscapular brown adipocytes in vivo

Xue, Kaili; Wu, Dongmei; Qiu, Yifu

doi:10.1016/j.xpro.2022.101895

Cited by 2 publications

(2 citation statements)

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“…The absence of MCU or Emre in brown adipose tissue (BAT) significantly impairs thermogenesis and exacerbates obesity and metabolic dysfunction. 76,108 BAT and WAT can be transformed into each other. 109,110 NAD-dependent deacetylase sirtuin-3 (SIRT3) inhibits MCU-mediated mitochondrial Ca 2+ overload by reducing histone H3K27ac levels at the MCU promoter in an AMPactivated protein kinase (AMPK)-dependent manner.…”

Section: Mcu Complex In Obesitymentioning

confidence: 99%

“…Brown adipose tissue can breakdown white adipose tissue, thus maintaining or reducing body weight, as well as alleviating obesity. The absence of MCU or Emre in brown adipose tissue (BAT) significantly impairs thermogenesis and exacerbates obesity and metabolic dysfunction 76,108 . BAT and WAT can be transformed into each other 109,110 .…”

Section: Pathological Role Of Mcu Complex In Metabolic Diseasesmentioning

confidence: 99%

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Implications of MCU complex in metabolic diseases

Li,

Sun,

Zhang

et al. 2023

The FASEB Journal

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Metabolic diseases are considered the primary culprit for physical and mental health of individuals. Although the diagnosis of these diseases is relatively easy, more effective and convenient potent drugs are still being explored. Ca 2+ across the inner mitochondrial membrane is a vital intracellular messenger that regulates energy metabolism and cellular Ca 2+ homeostasis and is involved in cell death. Mitochondria rely on a selective mitochondrial Ca 2+ unidirectional transport complex (MCU complex) in their inner membrane for Ca 2+ uptake. We found that the channel contains several subunits and undergoes dramatic transformations in various pathological processes, especially in metabolic diseases. In this way, we believe that the MCU complex becomes a target with significant potential for these diseases. However, there is no review linking the two factors, thus hindering the possibility of new drug production. Here, we highlight the connection between MCU complex-related Ca 2+ transport and the pathophysiology of metabolic diseases, adding understanding and insight at the molecular level to provide new insights for targeting MCU to reverse metabolism-related diseases.

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