China
Africa
Explore chapters and articles related to this topic
Signal transduction and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Brendan Egan, Adam P. Sharples
In a similar manner to proteolysis, autophagy is likely to be involved in skeletal muscle remodelling in response to exercise. Autophagy occurs through various mechanisms that differ in the way they capture proteins or organelles and deliver them to the lysosome for degradation. Macro-autophagy involves entire regions of the cytosol or specific organelles and protein complexes being engulfed by a vacuole known as an autophagosome, which then fuses with the lysosome. Micro-autophagy involves the direct uptake of cytosolic components into lysosomes. In addition, more selective types of autophagy, known as chaperone-mediated autophagy and chaperone-assisted selective autophagy, are able to degrade specific proteins. Like the concept of protein degradation by the UPS, on first impression, autophagy may seem highly destructive, but autophagic processes are initiated by a single session of exercise (77), and in fact may be required for adaptation to exercise training (78). Conceptually, this can be thought of acute exercise activating signal transduction pathways that increase the turnover of skeletal muscle proteins (i.e. activation of both degradation and synthesis), and this increase in turnover is essential for the remodelling of cellular components such as contractile proteins and the extracellular matrix that occurs with exercise training.
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
Autophagy is a controlled self-digestion involved in many H2 functions such as protein and organelle degradation [31]. Autophagy also protects cells against oxidative damage and innate pathogens. Furthermore, it is involved in antigen presentation as well as pathogen clearance and lymphocyte homeostasis. Three distinct types of autophagy have been identified: micro-autophagy, macro-autophagy, and chaperone-mediated autophagy (CMA) [31].
Role of Environmental Toxicants and Inflammation in Parkinson’s Disease
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Biddut Deb Nath, Dipti Debnath, Rokeya Pervin, Md. Akil Hossain
In LB, the presence of large proteins, particularly α-syn, leads to the notion that PD might interrupt the catabolism of mutated, undesired, or destroyed proteins resulting in neuronal mortality and cellular accumulation.31,95 Which contributed to the study of the lysosomes ubiquitin proteasome network (UPS) pathogenesis of PD functions. Mutations in UCH-L1 and Parkin endorsed participation of UPS, which serves as a ligase of ubiquitin protein and in the reprocessing of ubiquitin. Assessment of the 26S proteasome in PD disclosed specific modifications in its enzymatic performance and structure in the SNc that were presumably erroneously affiliated with disordered α-syn degeneration.96 In cultured cells, the introduction of cell death with proteasomal blockers has contributed to a series of events, including increased nitrative and oxidative stress, as well as modifications and destruction in mitochondrial activity.97 Admittedly, a strong correlation occurs between the 26S proteasome controlling caps, which are ATPases, and the mitochondrial electron transport function. Transcriptional microarray experiments on laser-captured, microdissected nigral dopaminergic neurons from PD have verified the possible function of the UPS.98 Conversely, the hypothesis lost legitimacy after a sluggish, gradual cerebral degradation in neurons mirrored PD was reported after the systematic administration of proteasomal blockers, although this was never repeated substantially.99 Therefore, focus switched to autophagy involving microautophagy, chaperone-mediated autophagy, and macroautophagy and lysosomes.88 Because LB has autophagosomes and autophagy-related proteins, it seemed a sustainable destination for dopaminergic cell death-related interruption. Admittedly, SNc in PD decreases the expression of heat shock protein 70, lysosome-correlated membrane protein type 2A (LAMP2A), and the chaperone-mediated autophagy proteins.100
DR1-CSE/H2S pathway upregulates autophagy and inhibits H9C2 cells damage induced by high glucose
Published in Acta Cardiologica, 2023
Hongzhu Li, Yaxin Wei, Yuxin Xi, Lijie Jiao, Xin Wen, Ren Wu, Guiquan Chang, Fengqi Sun, Jinghui Hao
Autophagy, a self-protection program, which is a process in which cells reuse their own substances through ‘self-eating’ [5]. According to the occurrence and mechanism, autophagy can be divided into chaperone-mediated autophagy, microautophagy, and macroautophagy [6]. Under physiological conditions, cell autophagy is involved in several biological effects, such as defense against microorganisms and starvation, metabolic support, etc [7,8]. AMP-activated protein kinase (AMPK)-mammalian Target of Rapamycin (mTOR) signaling pathway and phosphatidylinositol 3-kinase (PI3K)-protein kinase B (PKB/Akt)-mTOR signaling pathway are the two most classic signaling pathways of autophagy [9], while mTOR is a central negative regulator in the process of autophagy, which can regulate the activity of unc51-like kinase 1 (ULK1) complex and vacuolar protein sorting 34 (VPS34) complexes [10]. According to reports, hydrogen sulfide (H2S) can regulate autophagy through AMPK-mTOR and PI3K-Akt-mTOR signaling pathways [11,12].
Endostatin in fibrosis and as a potential candidate of anti-fibrotic therapy
Published in Drug Delivery, 2021
Zequn Zhang, Xi Liu, Zhaolong Shen, Jun Quan, Changwei Lin, Xiaorong Li, Gui Hu
Autophagy is the physiological catabolic mechanism that uses lysosomes to break down harmful cellular components, including misfolded proteins, damaged organelles, and excessive lipids, to achieve the clearance and reuse of cytoplasmic waste (Mizushima et al. 2008). Autophagy is a self-survival mechanism that occurs under special circumstances such as external stress, hunger, hypoxia, and endoplasmic reticulum stress. The disruption of the autophagy mechanism is closely related to the pathogenesis of tumors, neurodegenerative diseases, metabolic-related diseases, immune diseases, and other diseases (Levine & Kroemer 2019; Morishita & Mizushima 2019). Depending on the route of cargo transport into lysosomes, autophagy pathways are divided into three main categories: macroautophagy, microautophagy, and chaperone mediated autophagy; currently, macroautophagy has been the most extensively studied. Macroautophagy is characterized by autophagosomes that swallow excess cytoplasmic components and fuze with lysosomes; it is a multistep process that involves initiation, nucleation, expansion, fusion, and degradation (Dikic & Elazar 2018). In microautophagy, the lysosome membrane directly wraps the small cytosolic components without the assistance of autophagosomes (Oku & Sakai 2018). Chaperone-mediated autophagy refers to the process in which the proteins containing a specific motif are identified and combined by a chaperone and then translocated across the lysosomal membrane (Kaushik & Cuervo 2018).
The Controversial Role of Autophagy in Tumor Development: A Systematic Review
Published in Immunological Investigations, 2020
Bridilla Luiza Colhado Rodrigues, Maria Anete Lallo, Elizabeth Cristina Perez
The term autophagy was introduced by Christian De Duve in 1960s (Ávalos et al. 2014). It is defined as a natural biological process that plays a critical role in maintaining cellular homeostasis, degrading damaged or aged organelles and excess proteins (Chen and Karantza-Wadsworth 2009). Currently, three classes of autophagy are described: macroautophagy, microautophagy and chaperone-mediated autophagy (Bhattacharjee et al. 2019). Macroautophagy is the main route used to eliminate damaged macromolecules and organelles, characterized by authophagosome formation; a double membrane that fuses with a lysosome in order to degrade the constituent material inside. In microautophagy there is not authophagosome formation because cytosolic components are directly integrated into lysosomes by internal invagination of the lysosomal membrane. The chaperone-mediated autophagy is a complex and specific pathway that does not involve membrane reorganization, since substrate proteins directly translocate across the lysosomal membrane mediated by the recognition of Hsc70 chaperone protein (Hao et al. 2019). Among of three autophagy types, the macroautophagy, more commonly referred as autophagy has been the most extensively studied and is therefore, the best well characterized (Mizushima and Komatsu 2011; Wen and Klionsky 2016).