metabolism by affecting multiple cellular events in different organelles, including endoplasmic reticulum (ER) and mitochondria ( Meyer et al. 2013 , Nadal et al. 2017 , Rajamani et al. 2017 ). Mitochondria are essential for the normal cellular
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Laura Marroqui, Eva Tudurí, Paloma Alonso-Magdalena, Iván Quesada, Ángel Nadal, and Reinaldo Sousa dos Santos
Sergio Di Meo, Susanna Iossa, and Paola Venditti
dysregulation, including IR. The theory also suggests that mitochondria are key players in the IR development, but there are different views about the mechanisms by which mitochondria contribute to IR pathogenesis. It has been proposed that a decrease in
Yuehui Zhang, Min Hu, Wenyan Jia, Guoqi Liu, Jiao Zhang, Bing Wang, Juan Li, Peng Cui, Xin Li, Susanne Lager, Amanda Nancy Sferruzzi-Perri, Yanhua Han, Songjiang Liu, Xiaoke Wu, Mats Brännström, Linus R Shao, and Håkan Billig
activation of ferroptosis in the gravid uterus and placenta contribute to HAIR-induced fetal loss in both animal models and humans. Mitochondria play a protective role in the regulation of glutathione-induced ferroptosis ( Gao et al. 2019 ). In women with
Kechun Tang, Teresa Pasqua, Angshuman Biswas, Sumana Mahata, Jennifer Tang, Alisa Tang, Gautam K Bandyopadhyay, Amiya P Sinha-Hikim, Nai-Wen Chi, Nicholas J G Webster, Angelo Corti, and Sushil K Mahata
cristae membrane surface area. To normalize the measurement, this area was divided by the outer membrane area per mitochondrion. The sum of the area of the mitochondria was divided by the area of the cytoplasm and multiplied by 100 to determine the
Sandra Zárate, Mariana Astiz, Natalia Magnani, Mercedes Imsen, Florencia Merino, Silvia Álvarez, Analía Reinés, and Adriana Seilicovich
Introduction Mitochondria are key organelles for cellular bioenergetics and survival. They are the main source of ATP production through oxidative phosphorylation by the mitochondrial respiratory chain and also the primary sites for cellular
R Mastrocola, F Restivo, I Vercellinatto, O Danni, E Brignardello, M Aragno, and G Boccuzzi
role in brain damage ( Aragno et al. 2000 a , b , 2002 , Arvanitakis et al. 2004 ). Emerging evidence shows that the increased oxidative stress and consequent oxidative damage observed in hyperglycemic conditions begins in the mitochondria, which
Zhe-Zhen Liao, Xiao-Yan Qi, Ya-Di Wang, Jiao-Yang Li, Qian-Qian Gu, Can Hu, Yin Hu, Heng Sun, Li Ran, Jing Yang, Jiang-Hua Liu, and Xin-Hua Xiao
betatrophin in WAT beiging by employing a loss-of-function approach in mice. Here, we discovered that inhibition of betatrophin attenuated white fat mass and improve TG levels through stimulating beiging process and mitochondria biogenesis. The above process
Giuseppe Calamita, Maria Moreno, Domenico Ferri, Elena Silvestri, Patrizia Roberti, Luigi Schiavo, Patrizia Gena, Maria Svelto, and Fernando Goglia
Introduction Triiodothyronine (T3) exerts significant actions on energy metabolism, with mitochondria being a major target for its effects ( Soboll 1993 ). Extensive changes occur in the mitochondrial compartment in response either
Malin Fex, Lisa M Nicholas, Neelanjan Vishnu, Anya Medina, Vladimir V Sharoyko, David G Nicholls, Peter Spégel, and Hindrik Mulder
secretion by circulating hormones, paracrine and autocrine mechanisms and neuronal (autonomic and sensory) activity. All these mechanisms combine to enhance insulin secretion in an efficacious fashion ( Ahrén 2000 ). Here, mitochondria play a key role
Amanda J Genders, Jujiao Kuang, Evelyn C Marin, Nicholas J Saner, Javier Botella, Macsue Jacques, Glenn K McConell, Victor A Andrade-Souza, Javier Chagolla, and David J Bishop
. 2008 , Kunz et al. 2019 ), which were reported following an HFD. A potential factor contributing to these contrasting findings is that many of the studies have assessed mitochondrial respiratory function in isolated mitochondria ( Lionetti et al
