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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].
Apoptosis and Cell Death
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Macroautophagy is a process by which cytoplasm and organelles are engulfed into double membrane bound vesicles called autophagosomes (self-eating), which ultimately fuse with lysosomes for digestion and recycling of contents by lysosomal hydrolases. This process is utilized, for example, in situations of starvation, oxidative stress or hypoxia. Publications frequently specify that it is macroautophagy that is the form of autophagy being referred to (i.e. the use of autophagosomes to transport cargo to the lysosome) and then simply use the term ‘autophagy’ thereafter. Tumour cells are believed to utilize this process, promoting survival of tumour cells in unfavourable conditions. Autophagy contributes to chemotherapy resistance, for example in esophageal cancer cells treated with cisplatin or 5-fluorouracil.14 Some agents can induce excessive autophagy leading to cell death, but the consequence of autophagy can be context dependent and the microenvironment can adjust the threshold at which autophagy levels promote cell survival or cell death. There is now believed to be cross-talk between the processes of apoptosis, autophagy and ‘regulated/programmed necrosis’.15
Mitochondrial Oxidative Stress in Aging and Healthspan
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
Several cellular mechanisms are involved in proteostasis and protein quality control. Autophagy is one of the main mechanisms degrading the vast majority of proteins. The other mechanism includes ubiquitin–proteasome pathway. Autophagic degradation involves lysosomes, which contains several digestive enzymes.39 Three major pathways have been described based on the delivery mechanisms of macromolecules to the lysosome: microautophagy, macroautophagy, and chaperone-mediated autophagy (CMA).40 Microautophagy acts through invaginations of the lysosomal membrane directly engulfing cytoplasmic macromolecules into the lysosome followed by enzymatic degradation.40,41 Macroautophagy involves formation of autophagosomes, which are double-membrane vesicles formed by phagophores engulfing cytosolic proteins and organelles. These autophagosomes fuse with lysosomes, leading to the degradation of the sequestered cellular contents by lysosomal enzymes.42,43 CMA is a targeted degradation, in which cytosolic proteins containing a pentapeptide KFERQ motif are targeted and translocated across the lysosomal membrane, resulting in the degradation of specific proteins.44 These three mechanisms of autophagy may occur simultaneously in various cell types.39,45,46 Macroautophagy is the most extensively studied of these three mechanisms and will be the focus of the following discussion.
Autophagy in peripheral blood mononuclear cells is associated with body fat percentage
Published in Archives of Physiology and Biochemistry, 2023
Fabiano T. Amorim, Roberto C. Nava, Kurt A. Escobar, Zidong Li, Anna M. Welch, Zachary J. Fennel, Zachary J. McKenna, Ann L. Gibson
Macroautophagy (herein referred to as autophagy) is a catabolic cellular maintenance system responsible for the identification, degradation, and recycling of dysfunctional and damaged proteins, organelles, and intracellular pathogens (Yorimitsu and Klionsky 2005). The autophagic process involves the formation of double membrane vesicles called autophagosomes. These structures sequester damaged organelles and mis-folded proteins and fuse with lysosomes forming autolysosomes in which the cargo is degraded. The constituent products are then released into the cytoplasm for use in cellular processes, including production of new proteins and metabolism. This proteostatic system is activated by nutrient restriction and energetic challenge (Vainshtein and Hood 2016). Autophagy prevents the accumulation of deleterious cytosolic components and is essential for the maintenance of cellular homeostasis (Feng et al.2014). Dysregulation of autophagy has been implicated in many diseases including cardiovascular disease, obesity, and type II diabetes (Murrow and Debnath 2013).
Nano-titanium dioxide exposure and autophagy: a systematic review and meta-analysis
Published in Toxin Reviews, 2023
Li Li, Ruoyun Dong, Tao Liu, Yaqian Yang, Hongmei Chang, Xiaojia Meng, Yaxin Deng, Qianqian Wang, Yiman Zhao, Guanling Song, Yunhua Hu
There are three primary modes of autophagy: microautophagy, chaperone-mediated autophagy, and macroautophagy in mammalian cells (Parzych and Klionsky 2014). Cargos are engulfed and absorbed by lysosomes directly in a nonspecific manner, which is called microautophagy (Schuck 2020). For example, nano-TiO2 can directly enter lysosomes and be degraded (De Matteis et al.2016). Cargo proteins contain a particular KFERQ-like motif, which are recognized by molecular chaperones. These proteins can cross membrane of lysosomes through dedicated translocation complexes, which is called chaperone-mediated autophagy (Kaushik and Cuervo 2018). Among the three types of autophagy, macroautophagy is major and the most typical pathway for degradation. During this process, double-membrane sequestering compartments containing cargoes are formed, which are called phagophore, and they will become autophagosomes after maturation, and then these cargoes will be degraded after autophagosomes bind with lysosomes (Nguyen et al.2020). This meta-analysis primarily focuses on the influence of nano-TiO2 on macroautophagy process.
Bryonia multiflora Extract Induces Autophagy via Regulating Long Non-coding RNAs in Breast Cancer Cells
Published in Nutrition and Cancer, 2021
Onur Tokgun, Pervin Elvan Tokgun, Samet Turel, Behcet Inal, Kubilay Inci, Secil Tan, Ozge Can Alvur
High expression of lncRNA-p21 is reported to be associated with promoted proliferation, motility, reduction of apoptosis, and induction of autophagy in hepatoma and glioma cells by way of HIF-1/Akt/mTOR/P70S6K pathways [27]. Moreover, it has already been shown that lincRNA p21 negatively regulates apoptosis in NSCLC [56]. lincRNA-p21 promotes its neighboring gene p21 in the nucleus. p21 is also considered to be a critical component of the senescence response pathway [57]. We observed that MDA-MB-231 cells showed decreased levels of lincRNA-p21 with increased levels of p21 mRNA, but in MCF-7 cells, there were increased expression levels for both LincRNA-p21 and p21 mRNA levels. There is growing evidence for the connection between p21 and macroautophagy. Different results have emerged regarding the modulation of macroautophagy. It has been shown that overexpression of p21 induces macroautophagy and senescence in breast cancer cells. Our study has been demonstrated that p21 levels are increased after BMST treatment, indicating that both autophagy and senescence are induced in MCF-7 and MDA-MB-231 breast cancer cells.