Autophagy: The Powerful of Immune Response
| dc.contributor.author | Mosab Nouraldein Mohammed Hamad | |
| dc.date.accessioned | 2023-10-15T06:55:38Z | |
| dc.date.available | 2023-10-15T06:55:38Z | |
| dc.date.issued | 2019-12-29 | |
| dc.description.abstract | Introduction Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome. Despite its simplicity, recent progress has demonstrated that autophagy plays a wide variety of physiological and pathophysiological roles, which are sometimes complex. Autophagy consists of several sequential steps sequestration, transport to lysosomes, degradation, and utilization of degradation products and each step may exert different function. This process is quite distinct from endocytosis-mediated lysosomal degradation of extracellular and plasma membrane proteins. There are three types of autophagy macroautophagy, micro autophagy, and chaperone-mediated autophagy and the term “autophagy” usually indicates macroautophagy unless otherwise specified. Autophagy is mediated by a unique organelle called the autophagosome. As autophagosomes engulf a portion of cytoplasm, autophagy is generally thought to be a nonselective degradation system. This feature is in marked contrast to the ubiquitin-proteasome system, which specifically recognizes only ubiquitinated proteins for proteasomal degradation. It is therefore reasonable to assume that the ubiquitin-proteasome system has numerous specific functions because it can selectively degrade thousands of substrates. Recent studies have clearly demonstrated that autophagy has a greater variety of physiological and pathophysiological roles than expected, such as starvation adaptation, intracellular protein and organelle clearance, development, anti-aging, elimination of microorganisms, cell death, tumor suppression, and antigen presentation. Additionally, in some situations, the contribution of autophagy seems to be very complicated. For example, it is very difficult to generalize the role of autophagy in cancer and cell death [1]. | |
| dc.identifier.uri | https://ds.eaeu.edu.sd/handle/10.58971/78 | |
| dc.language.iso | en | |
| dc.publisher | Medcrave | |
| dc.title | Autophagy: The Powerful of Immune Response | |
| dc.type | Book | |
| dcterms.abstract | ntroduction Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome. Despite its simplicity, recent progress has demonstrated that autophagy plays a wide variety of physiological and pathophysiological roles, which are sometimes complex. Autophagy consists of several sequential steps sequestration, transport to lysosomes, degradation, and utilization of degradation products and each step may exert different function. This process is quite distinct from endocytosis-mediated lysosomal degradation of extracellular and plasma membrane proteins. There are three types of autophagy macroautophagy, micro autophagy, and chaperone-mediated autophagy and the term “autophagy” usually indicates macroautophagy unless otherwise specified. Autophagy is mediated by a unique organelle called the autophagosome. As autophagosomes engulf a portion of cytoplasm, autophagy is generally thought to be a nonselective degradation system. This feature is in marked contrast to the ubiquitin-proteasome system, which specifically recognizes only ubiquitinated proteins for proteasomal degradation. It is therefore reasonable to assume that the ubiquitin-proteasome system has numerous specific functions because it can selectively degrade thousands of substrates. Recent studies have clearly demonstrated that autophagy has a greater variety of physiological and pathophysiological roles than expected, such as starvation adaptation, intracellular protein and organelle clearance, development, anti-aging, elimination of microorganisms, cell death, tumor suppression, and antigen presentation. Additionally, in some situations, the contribution of autophagy seems to be very complicated. For example, it is very difficult to generalize the role of autophagy in cancer and cell death [1]. Macroautophagy (hereafter autophagy), or ‘self-eating’, is a conserved cellular pathway that controls protein and organelle degradation, and has essential roles in survival, development and homeostasis. Autophagy is also integral to human health and is involved in physiology, development, lifespan and a wide range of diseases, including cancer, neurode generation and microbial infection. Although research on this topic began in the late 1950s, substantial progress in the molecular study of autophagy has taken place during only the past 15 years. This review traces the key findings that led to our current molecular understanding of this complex process. The term ‘autophagy’ comes from the Greek words ‘phagy’ meaning eat, and ‘auto’ meaning self. Autophagy is an evolutionarily conserved process in eukaryotes by which cytoplasm cargo sequestered inside double-membrane vesicles are delivered to the lysosome for degradation. When autophagy was initially discovered more than 40 years ago, it was perplexing as to why the cell would self-digest its own components. The simplest hypothesis was that autophagy serves as a cellular rubbish-disposal mechanism. However, we have since learnt that this ‘self-eating’ process not only rids the cell of intracellular misfolded or long-lived proteins, superfluous or damaged organelles, and invading microorganisms, but also is an adaptive response to provide nutrients and energy on exposure to various stresses. Autophagy has been connected to human pathophysiology, and continued expansion of our knowledge about autophagy has had implications for fields as wide-ranging as cancer, neurodegeneration, immune response, development and ageing. This timeline reviews the history of autophagy research with a focus on the key events that occurred over the past 15 years, when our molecular understanding of this process first began. |
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