China
Africa
Explore chapters and articles related to this topic
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].
Etiopathogenesis
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
Dario Didona, Biagio Didona, Giovanni Paolino, Raffaele Dante Caposiena Caro
Both micro- and macro-autophagy are involved in engulfing large structures through both selective and nonselective mechanisms. On the other hand, CMA degrades only soluble proteins in a selective way [32]. In macro-autophagy, a multimembrane structure known as a phagophore engulfs the cytoplasmic organelles, producing a vesicular structure called an autophagosome. Subsequently, the autophagosome fuses with the lysosome, forming a single membrane structure called an autolysosome [31]. On the other hand, micro-autophagy is characterized by direct engulfing of organelles, involving a process of invaginating, protrusion, and/or septation of the lysosomal-limiting membrane [32]. Instead, CMA involves the 70 KDa heat shock-cognate protein and the lysosomal-associated membrane protein 2A receptor (LAMP2A) to transport specific cytosolic proteins, all characterized by pentapeptide sequence Lys-Phe-Gln-Arg-Gln, into lysosomes [32].
Pathogenesis of Tuberculosis
Published in Lloyd N. Friedman, Martin Dedicoat, Peter D. O. Davies, Clinical Tuberculosis, 2020
Divya B. Reddy, Jerrold J. Ellner
Autophagy is a homeostasis pathway wherein discrete portions of the cytoplasm are sequestered into an “autophagosome,” and delivered to lysosomes for degradation. Gutierrez and Singh have demonstrated that induction of autophagic pathways by drugs such as rapamycin can enhance host resistance to MTB by promoting phagosome maturation. In fact, IFN-γ-induced activation of p47 GTPases such as LRG-47 in MTB-infected macrophages leads to formation of large organelles with autophagolysosomal properties and in part, explains the reactive nitrogen- and oxygen-independent pathways of IFN-γ antimicrobial action.51 Similarly, Yuk et al. have shown that vitamin D3 exhibits antimycobacterial properties, by inducing autophagy in human monocytes via cathelicidin driven transcription of the autophagy-related genes Beclin-1 and Atg5.52 The role of autophagy in controlling bacterial burden and limiting tissue damaging inflammation is now becoming apparent and it is potentially a pathway for pharmacological manipulation.53
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).
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].
An exploratory investigation of apoptotic and autophagic responses in peripheral blood mononuclear cells following maximal aerobic exercise in obese individuals
Published in Archives of Physiology and Biochemistry, 2022
Chun-Jung Huang, Alexandra L. Rodriguez, Nishant P. Visavadiya, Brandon G. Fico, Aaron L. Slusher, Peter J. Ferrandi, Michael Whitehurst
Autophagy is a molecular process that functions as a disposal system in the elimination of damaged organelles (Deretic et al.2013) while also serving as an imperative regulator of cellular metabolism and homeostasis via the engulfment of autophagosomes by autophagy-related (ATG) proteins (Ryter et al.2013; Zada et al.2015). Specifically, Yang et al. (2010) have demonstrated that hepatic autophagy proteins, including ATG5, ATG7, and beclin1 are downregulated following a high-fat diet (HFD) in mice (Yang et al.2010). Furthermore, hepatic autophagy, indicated by the ratio of LC3-II/LC3-I, is also reduced with insulin resistance and hyperinsulinemia in HFD-induced mice (Liu et al.2009). However, exercise-induced autophagy has been shown to enhance glucose uptake in skeletal muscle (He et al.2012) and protect β cells against endoplasmic reticulum stress-induced apoptosis in mice (Sarparanta et al.2017). Taken together, these findings support the protective role of autophagy as a critical regulator of insulin action against diabetic complications in obesity. While autophagy has been recently discovered as a critical molecular process in promoting cell survival against apoptosis, particularly with aging (Fernández et al.2018), the mechanisms of obesity-induced apoptosis still remain yet to be elucidated.