Systems biology of the autophagy-lysosomal pathway

MicroRNA

“…Jegga et al proposed that miR-130, miR-98, miR-124, miR-204 and miR-142 have potential regulatory functions in the autophagic process based on computational analysis. 19 Later, miR-130a was shown to inhibit autophagic flux in chronic lymphocytic leukemia (CLL) cells by decreasing the expression level of its targets, ATG2B and DICER1, which are essential for autophagosome formation. 20 …”

New Insight in The Molecular Mechanisms of Neurodegenerative Disease

“…(153,188,189) Furthermore, studies have found that autophagy and lysosomal gene expression may be coordinately regulated at transcriptional and post-transcriptional levels, and that genetic mutations of autophagy genes lead to abnormal cell and tissue homeostasis. (190)(191)(192)(193) It is well recognized that mitochondrial dysfunction and increased oxidative stress play important roles in brain aging and the development of NDDs. Our recent findings that decreased mTOR signaling and dietary restriction are novel stimuli for mitochondrial localization of TERT protein, and the role of the telomerase protein TERT in brain on lowering mitochondrial ROS in an mTOR signaling dependent manner, therefore identify new players and connections in an ever bigger network of signaling events in the brain.…”

Introductory Chapter: Overview on Autophagy in Burden of Functions

“…4]. Overall, that phenomena make the autophagy-lysosomal pathway to be a universal mechanism for decomposition of biological targets regardless their biochemical nature yet vital for response to stress and damage [1,2]. The functional role of the autophagy machinery in immunochemical and structural cellular homeostasis can be further elaborated within a framework of "entity component system architecture" with a perspective on "the autophagy-mediated intrinsic barrier network".…”

“…Remarkably, often the same mechanisms orchestrate response to impacts of environmental and oxidative stressogens, toxins and adverse conditions caused by a variety of infections, and degenerative and malignant transformations. Among these mechanisms, a crucial role is borne by autophagy-lysosomal catabolicmachinery or autophagy, which is constituted by a large interactome of autophagy-related genes and organelle networks, that is integrated within a distinct singularity along with newly introduced "omes" such as "exposome" and "stressome" [1][2][3][4][5]. The normal "housekeeping task burden" of the autophagy system (i.e., chaperone-mediated autophagy, microautophagy and the nonselective and selective macroautophagy) is to sustain, adjust, reconstitute and to remodel the cellular contents in order to maintain cell metabolism, phenotypes and structural integrity, especially in the case of starvation when energy molecules are depleted, nutrition is limited, and thus death risk is high [2,5].…”

“…Among these mechanisms, a crucial role is borne by autophagy-lysosomal catabolicmachinery or autophagy, which is constituted by a large interactome of autophagy-related genes and organelle networks, that is integrated within a distinct singularity along with newly introduced "omes" such as "exposome" and "stressome" [1][2][3][4][5]. The normal "housekeeping task burden" of the autophagy system (i.e., chaperone-mediated autophagy, microautophagy and the nonselective and selective macroautophagy) is to sustain, adjust, reconstitute and to remodel the cellular contents in order to maintain cell metabolism, phenotypes and structural integrity, especially in the case of starvation when energy molecules are depleted, nutrition is limited, and thus death risk is high [2,5]. In these events, autophagy biogenesis is regulated with precision by the autophagyresponse receptors and signaling systems at metabolic and immune checkpoints that operate in conjunction with other cellular elements and machineries, such as cellular energy sensors, the proteotoxic stress sensors the pattern recognition receptors, the ubiquitin system, galectins, danger and redox signaling cascades, the endoplasmic reticulum-mitochondrial system, etc.…”