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Nanoparticles and Viruses as Mitophagy Inducers in Immune Cells
Published in Bertrand Henri Rihn, Biomedical Application of Nanoparticles, 2017
Housam Eidi, Zahra Doumandji, Lucija Tomljenovic, Bertrand Henri Rihn
Recently, cell or mitochondria/NP interactions are considered as another possible cause of mitochondrial dysfunction as NPs affect mitochondrial biology either directly (physical interaction) or indirectly (biochemically). As mentioned above, mitochondria can be a specific intercellular target for several kinds of NPs, resulting in important morphological changes, such as a serious damage in the mitochondrial cristae structure and alteration of their double membrane integrity (Figure 6.6; Eidi et al. 2012). NPs that do not have any tendency to penetrate into mitochondria could affect mitochondria biology indirectly via different biochemical pathways, especially oxidative stress and gene expression. Mitochondrial morphology and membrane integrity are important mitochondrial responses to stress signals. Furthermore, mitochondria are seen as dynamic intracellular organelles that continually undergo opposing morphological changes, fusion and fission, as a response to different signals (Barbour and Turner 2014). In the fusion process, several mitochondria form unique elongated mitochondria, while in fission, a single mitochondrion is fragmented into many smaller ones (Figure 6.6b). Mitochondrial morphology changes can be induced as a result of mitochondrial stress and may be a mechanism of homeostasis to regulate cell survival. Mitochondrial fusion generally is seen as a response to mitochondrial damage and elongated mitochondria are considered a pro-survival process resulting in prevention of apoptotic cell death and mitophagy (Barbour and Turner 2014). Mitochondrial fusion can be induced by oxidative stress (Barbour and Turner 2014) resulting in increased resistance to ROS (Wang et al. 2013). However, mitochondrial fission can be generated by different cell stressors, such as mitochondria/NPs interaction, inducing mitophagy and programmed cell death (Eidi et al. 2012).
Computation of the mitochondrial age distribution along the axon length
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
Ivan A. Kuznetsov, Andrey V. Kuznetsov
Renewal of mitochondrial proteins involves mitochondrial fusion and fission (Misgeld and Schwarz 2017). Fusion of old and new mitochondria leads to an exchange of old and new soluble and membrane-bound components, such as mitochondrial proteins (Malka et al. 2005; Patel et al. 2013). It is believed that mitochondrial fission leads to the separation of mutated copies of the mitochondrial genome into a separate mitochondrion, which is then recycled by the autophagosome (Twig et al. 2008; Safiulina and Kaasik 2013). Fission also serves as a mechanism that prevents mitochondria from becoming excessively long, so longer mitochondria are more likely to enter fission than shorter ones (Cagalinec et al. 2013). If fission events are unopposed, they can lead to complete fragmentation of the mitochondrial network (Ahola et al. 2019). Mitochondrial fusion accelerates mitochondrial fission, which is necessary to maintain a constant average length of mitochondria. Fission is important for autophagy, the mechanism of mitochondria removal (Twig et al. 2008).