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Mitochondrial Dysfunction in Huntington Disease
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Md. Hafiz Uddin, Marufa Rumman, Tasnuva Sarowar
The lack of balance between mitochondrial fission and fusion negatively affects mitochondrial turnover. Autophagy, as previously referred, is an important intracellular mechanism that removes damaged organelles and misfolded/aggregated proteins to maintain cell homeostasis (Carvalho et al. 2015). Autophagy is characterized by the presence of autophagic vacuoles, autophagosomes (Kamat et al. 2014). An optimal level of autophagy is essential for recycling cellular organelles, which provides neuroprotection. However, increased autophagy is detrimental, causing neuronal degeneration (Kamat et al. 2014; Jing and Lim 2012; Wong and Cuervo 2010; Liu et al. 2009). Autophagy can be divided into two broad categories, namely, microautophagy and macroautophagy. In microautophagy, the lysosome directly engulfs intracellular smaller molecules and is independent of nutritional deprivation (Filosto et al. 2011). On the other hand, in macroautophagy, autophagosome is formed with intracellular larger molecules. This is then fused with the lysosome to generate autophagolysosome and undergoes subsequent degradation. Macroautophagy of mitochondria is termed as mitophagy [74,75].
Exercise Training, Mitochondrial Adaptations, and Aging
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Nashwa Cheema, Matthew Triolo, David A. Hood
The selective degradation of mitochondria utilizing the autophagy–lysosome system is termed mitophagy. Preceding the breakdown of these organelles, damaged mitochondrial segments are removed from the network of mitochondria through fission (122, 170). Following fission, a multistep process ensues. Briefly, this includes organelle targeting, engulfment in a double membrane autophagosome, and finally transport to and degradation within the lysosome (165).
Mitochondrial Dysfunction in the Pathophysiology of Alzheimer’s Disease
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Mitophagy is the process through which severely damaged and/or dysfunctional mitochondria are identified and selectively degraded and recycled [60]. It is crucial for cellular homeostasis and it is impaired in AD [61–63] where mitochondria have been shown to be key targets of increased autophagic degradation [12]. Excess ROS can trigger autophagy [64] and dysfunctional mitochondria that overproduce ROS, are indeed selectively targeted for mitophagy [65]. Central to mitochondrial and cellular homeostasis, mitophagy is modulated by the PTEN-induced putative kinase 1 (PINK1)/Parkin pathway [66] which primarily targets mitochondria devoid of membrane potential (ΔΨm). Damaged mitochondria can also, independently of Parkin, increase FUNDC1 and Nix expression to recruit autophagosomes to mitochondria via direct interaction with LC3 [67,68]. Ubiquitin ligases, like Smurf1, target depolarized mitochondria for mitophagy [69–71].
Identification of Rab7 as an autophagy marker: potential therapeutic approaches and the effect of Qi Teng Xiao Zhuo granule in chronic glomerulonephritis
Published in Pharmaceutical Biology, 2023
Xiujuan Qin, Huiyu Chen, Xiaoli Zhu, Xianjin Xu, Jiarong Gao
Mitochondria are important eukaryotic cell organelles; they produce ATP via oxidative phosphorylation and provide 95% of the cell’s energy requirements. They are also involved in metabolic signal transduction, inflammation, and apoptosis regulation. The kidney is rich in mitochondria, which play a key role in its function, and mitochondrial damage and dysfunction are major factors in many chronic and acute kidney diseases (Tang et al. 2021). Maintaining mitochondrial homeostasis and metabolic balance is crucial for kidney function (Bhargava and Schnellmann 2017). When mitochondrial damage and dysfunction occur, mitophagy is induced to maintain cell homeostasis, removing damaged or excess mitochondria (Su et al. 2023). Transmission electron microscopy showed that abnormal mitochondrial cristae and decreased autophagosomes were apparent in the model group. Interestingly, we also found that mitochondrial damage was reduced after QTXZG treatment.
The role of autophagy in acute myeloid leukemia development
Published in Expert Review of Anticancer Therapy, 2023
Martyna Bednarczyk, Karolina Kociszewska, Olga Grosicka, Sebastian Grosicki
Several forms of autophagy have been identified: macrophagy, chaperone-related autophagy, microphagy, and specific autophagy (e.g. mitophagy). In all types of autophagy, the cytosolic components are degraded in the lysosomes in a proteolytic manner. All types of autophagy differ in terms of their physiological functions and the way in which the load is delivered to the lysosome. In macrophagy, the components for degradation are delivered to the lysosome via the autophagolysosome, which binds to the lysosome to form the autolysosome. In micro-autophagy, cytosolic components are directly taken up by the lysosome itself through invagination of the lysosomal membrane. In chaperone-dependent autophagy, proteins are translocated across the lysosomal membrane in a complex with chaperones (HSC70) that are recognized by the LAMP2A receptor located in the lysosome membrane. In turn, selective autophagy (e.g. mitophagy) is a type of macrophage, but it concerns specific structures and organelles that are to be degraded, in this case these are the mitochondria [19].
Banxia-Houpu decoction diminishes iron toxicity damage in heart induced by chronic intermittent hypoxia
Published in Pharmaceutical Biology, 2022
Ji-Xian Song, Ya-Shuo Zhao, Ya-Qin Zhen, Xin-Yue Yang, Qi Chen, Ji-Ren An, En-Sheng Ji
Mitophagy is defined as a critical endogenous cellular degradative process responsible for removing damaged mitochondria or mitochondrial proteins (Jahng et al. 2019). Mitochondrial damage, increased ROS or mitochondrial depolarization may lead to the stabilization and accumulation of PINK1 on the outer mitochondrial membrane (OMM), which activates the recruitment of Parkin from the cytosol to the mitochondrial membrane (Sciarretta et al. 2018; Doblado et al. 2021). Once Parkin is recruited or activated, some mitochondrial proteins will be ubiquitinated, conjugate p62, and then recruit the autophagosome membrane via LC3, eventually resulting in autophagy (Gottlieb and Thomas 2017; Tang et al. 2019) (Figure 8). Excessive or dysfunctional autophagy leads to an increase in free iron and even regulates cell death, such as ferroptosis (Liu et al. 2020). Iron treatment has been demonstrated to induce autophagy in vitro transiently; however, prolonged iron overload would lead to autophagy defects (Jahng et al. 2019). Therefore, it is vital to maintain the dynamic balance of iron in response to stress damage.