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Lysosomal Ion Channels and Human Diseases
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Peng Huang, Mengnan Xu, Yi Wu, Xian-Ping Dong
Autophagy is a lysosome-dependent cellular process for the turnover of organelles and molecules. It is predominantly a cell-survival mechanism, playing a critical role in cell growth, cell proliferation and differentiation, and tissue homeostasis and development (Klionsky et al., 2016; Levine and Kroemer, 2008; Mizushima and Levine, 2010). Cellular stress conditions such as nutrient and energy deprivation and diseases elevate autophagy. During autophagy, cytoplasmic components are engulfed by autophagosomes that fuse with lysosomes where cytoplasmic components are degraded by lysosomal hydrolases and then recycled. Autophagic flux is regulated by a series of events, including autophagy initiation, autophagosome-lysosome fusion (autophagosome maturation), autolysosome degradation, and lysosome reformation (Klionsky et al., 2016; Yu et al., 2010). Disruption of any of them could lead to impaired autophagy that has been associated with abnormalities such as LSDs, neurodegeneration, cancer, and inflammatory, infectious and autoimmune conditions (Fulda and Kogel, 2015; Hara et al., 2006; Komatsu et al., 2006; Levine and Kroemer, 2008; Levine et al., 2011). Basal autophagy is especially important in postmitotic cells such as neurons and muscles, where the accumulation of aggregated proteins and damaged organelles often results in cell death (Hara et al., 2006; Komatsu et al., 2006; Levine and Kroemer, 2008). Indeed, the suppression of basal autophagy causes neurodegeneration (Hara et al., 2006; Komatsu et al., 2006) and myofiber degeneration and weakness (Masiero et al., 2009; Raben et al., 2008).
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].
Alternative drug combination to treat chronic myeloid leukemia resistance in developing countries
Published in Ade Gafar Abdullah, Isma Widiaty, Cep Ubad Abdullah, Medical Technology and Environmental Health, 2020
A.F. Sumantri, A. Oehadian, M.H. Bashari
Various molecular and genetic mechanisms in CML cases are basic for the formation of TKI resistance mechanisms: one of them is the mechanism of CML stem cells. One of the mechanisms in CML stem cells causing resistance is the autophagy mechanism. Autophagy is a process of recycling a cell under conditions of stress (hypoxia, malnutrition, drug therapy, etc.), thus causing a cell to survive in these conditions. One drug that is known to function as an anti-autophagy agent is chloroquine (Hamad 2013, Mukhopadhyay 2016).
Identification of a new structural family of SGK1 inhibitors as potential neuroprotective agents
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Ines Maestro, Enrique Madruga, Patricia Boya, Ana Martínez
In addition, the role of SGK1 in autophagy is being explored9. Autophagy is a degradative process, by which cytoplasmic content is sequestered in a double-membrane structure, called autophagosome. The autophagosome will fuse with lysosomes, where the cargo is degraded18. As mTORC2 participates in SGK1 activation and inhibits autophagy19, SGK1 could be considered as a negative regulator of the pathway20. In fact, autophagy was upregulated in muscle in SGK1-deficient mice21. Thus, the inhibition of the kinase by the compound GSK650394 induced autophagy22,23. However, a recent work done in HEI-OC1, a mouse auditory cell line, showed an upregulation of SGK1 and autophagy when cells were treated with caffeine. This event was inhibited when cells were co-treated with the inhibitor GSK65039424. Thus new studies are needed to unravel the autophagy modulation by SGK1.
Astaxanthin delays brain aging in senescence-accelerated mouse prone 10: inducing autophagy as a potential mechanism
Published in Nutritional Neuroscience, 2023
Min Fu, Xiaoshan Liang, Xuguang Zhang, Mingzhe Yang, Qi Ye, Yuxuan Qi, Huan Liu, Xumei Zhang
Brain aging is a complex biological process often associated with a decline in motility and cognitive functions [1,2]. Age-associated dysfunction of the brain leads to severe health problems in the current aging society. Astaxanthin (AST) is mainly derived from Haematococcus pluvialis (H. pluvialis), has the characteristics of rapidly passing through the blood–brain barrier, and has a wide range of neuroprotective effects [3]. Its conjugated double bonds, hydroxyl and keto groups give it strong antioxidant properties [4], which has gained attention in combating aging [5]. A recent review reported that AST could regulate autophagy in heart, kidney, liver and lung [6]. Autophagy is a catabolic process, which improves cell microcirculation by phagocytizing damaged organelles in cells [7]. The lack of autophagy leads to the accumulation of mutant and misfolded proteins in cells, which underlie the emergence and development of neurodegenerative diseases and other aging-related diseases [8]. It will be important to delay aging and improve the health of the elderly by regulating autophagy. However, there are few studies on whether AST can affect brain aging by regulating autophagy.
Biosynthesis of silver nanoparticles using Citrus hystrix leaf extract and evaluation of its anticancer efficacy against HeLa cell line
Published in Drug Development and Industrial Pharmacy, 2022
Swetha Srimurugan, Anjali K. Ravi, Vijaya Anand Arumugam, Saradhadevi Muthukrishnan
Cervical cancer persists as the second major malignancy among women, with an annual global incidence of 570,000 diagnosed cases and 311,000 fatalities [1]. Human papilloma virus (HPV) infection is regarded as the major causative agent for the development of cervical cancer. Other risk factors include poor hygiene conditions, smoking, oral contraceptive usage, lifestyle changes, lack of physical activity, and exposure to radiation [2]. Since the inadequate preventive screening methods and early diagnosis, cervical cancer becomes aggressive and metastasizes into various parts [3]. The autophagy and apoptosis pathways maintain cellular homeostasis, but cancer cells become resistant to these pathways via modifying the anti and pro-apoptotic proteins to induce proliferation and metastasis of cancer cells [4]. Autophagy is a dynamic process associated with the formation of autophagosome, a double-membrane cytoplasmic vesicle which engulfs the damaged cellular components. The autophagosome can combine with lysosomes to generate auto-lysosomes, which preferentially destroy damaged cellular organelles and proteins by interacting with phosphatidyl ethanolamine, ATG 3, and ATG7 [5]. In normal circumstances, Beclin1 initiates autophagy by recruiting several autophagy-related complex proteins involved in autophagosome initiation and elongation. These protein complexes attract LC-3 I, which then transforms into LC-3 II [6].