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受损线粒体的排出和巨噬细胞的清除确保棕色脂肪组织中高效产热
2022-03-27 14:23

意大利罗马二大Daniele Lettieri-Barbato、Katia Aquilano等研究人员合作发现,受损线粒体的排出以及巨噬细胞对其的清除确保棕色脂肪组织(BAT)的高效生热作用。相关论文于2022年3月18日在线发表在《细胞—代谢》杂志上。

研究人员证明产热压力下的棕色脂肪细胞会释放细胞外囊泡(EV),其中含有氧化受损的线粒体部分以避免生热程序的失效。当被亲代棕色脂肪细胞重新吸收时,线粒体释放的EV减少了过氧化物酶增殖体激活受体-γ信号和线粒体蛋白的水平,包括UCP1。驻扎在BAT的巨噬细胞会通过吞噬活动来清除这些EV,有助于保护BAT的生理功能。体内巨噬细胞的耗竭导致BAT细胞外线粒体囊泡的异常积累,损害了对冷暴露的生热反应。这些发现揭示了组织驻留的巨噬细胞在BAT线粒体质量控制中的平衡作用。

据悉,最近的研究结果表明,线粒体可以在细胞间转移以控制代谢平衡。尽管棕色脂肪细胞的线粒体占细胞体积的很大一部分,并进行重组以维持产热,但目前仍不清楚BAT是否发生细胞间线粒体转移并调节适应性产热。

附:英文原文

Title: Ejection of damaged mitochondria and their removal by macrophages ensure efficient thermogenesis in brown adipose tissue

Author: Marco Rosina, Veronica Ceci, Riccardo Turchi, Li Chuan, Nicholas Borcherding, Francesca Sciarretta, María Sánchez-Díaz, Flavia Tortolici, Keaton Karlinsey, Valerio Chiurchiù, Claudia Fuoco, Rocky Giwa, Rachael L. Field, Matteo Audano, Simona Arena, Alessandro Palma, Federica Riccio, Farnaz Shamsi, Giovanni Renzone, Martina Verri, Anna Crescenzi, Salvatore Rizza, Fiorella Faienza, Giuseppe Filomeni, Sander Kooijman, Stefano Rufini, Antoine A.F. de Vries, Andrea Scaloni, Nico Mitro, Yu-Hua Tseng, Andrés Hidalgo, Beiyan Zhou, Jonathan R. Brestoff, Katia Aquilano, Daniele Lettieri-Barbato

Issue&Volume: 2022-03-18

Abstract: Recent findings have demonstrated that mitochondria can be transferred between cellsto control metabolic homeostasis. Although the mitochondria of brown adipocytes comprisea large component of the cell volume and undergo reorganization to sustain thermogenesis,it remains unclear whether an intercellular mitochondrial transfer occurs in brownadipose tissue (BAT) and regulates adaptive thermogenesis. Herein, we demonstratedthat thermogenically stressed brown adipocytes release extracellular vesicles (EVs)that contain oxidatively damaged mitochondrial parts to avoid failure of the thermogenicprogram. When re-uptaken by parental brown adipocytes, mitochondria-derived EVs reducedperoxisome proliferator-activated receptor-γ signaling and the levels of mitochondrialproteins, including UCP1. Their removal via the phagocytic activity of BAT-residentmacrophages is instrumental in preserving BAT physiology. Depletion of macrophagesin vivo causes the abnormal accumulation of extracellular mitochondrial vesicles in BAT,impairing the thermogenic response to cold exposure. These findings reveal a homeostaticrole of tissue-resident macrophages in the mitochondrial quality control of BAT.

DOI: 10.1016/j.cmet.2022.02.016

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(22)00088-2

Cell Metabolism:《细胞—代谢》,创刊于2005年。隶属于细胞出版社,最新IF:31.373
官方网址:https://www.cell.com/cell-metabolism/home
投稿链接:https://www.editorialmanager.com/cell-metabolism/default.aspx


本期文章:《细胞—代谢》:Online/在线发表

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