1. Signaling Pathways
  2. Autophagy

Autophagy

Autophagy 相关靶点 (followed by the number of products) :

Autophagy Autophagy
 × 

Autophagy

Related Products

PDF 5.23 MB

Overview of Autophagy:

Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome. Autophagy plays a wide variety of physiological and pathophysiological roles. Different selective forms of autophagy have been identified and characterized, leading to the specific degradation of organelles or pathogens. These selective pathways include the autophagic degradation of mitochondria (mitophagy), peroxisomes (pexophagy), endoplasmic reticulum (reticulophagy or ER-phagy), ribosomes (ribophagy), protein aggregates (aggrephagy), lipid droplets (lipophagy), spermatozoon-inherited organelles following fertilization (allophagy), secretory granules within pancreatic cells (zymophagy), or intracellular pathogens (xenophagy).

Autophagy consists of several sequential steps--sequestration, transport to lysosomes, degradation, and utilization of degradation products--and each step may exert different function. Autophagy signal transduction are mainly regulated by autophagy-related genes/proteins, Atgs. ATGs have unveiled much of the machinery of autophagosome formation. Furthermore, different non-ATG proteins are involved in the regulation and process of autophagy, e.g., mTOR, AMPK, AKT, AMBRA1, BCL2, DFCP1, or VPS34.

Autophagy and its dysregulation have been implicated in different human diseases or processes, such as cancer, neurodegeneration, immunity, or aging. Plenty of drugs and natural products are involved in autophagy modulation, either inducing or inhibiting autophagy, through multiple signaling pathways. Small molecules that can regulate autophagy seem to have great potential to modulate the clinical course of neurodegenerative diseases or promote chemotherapeutic response in tumor models. Besides, several clinical drugs and compounds in diabetes are also found to involve regulation of autophagy.

 

References:

[1] Glick D, et al. J Pathol. 2010 May;221(1):3-12.

[2] Mizushima N. Genes Dev. 2007 Nov 15;21(22):2861-73.

[3] Wesselborg S, et al。 Cell Mol Life Sci。 2015 Dec;72(24):4721-57。

[4] Zhang XW, et al。 J Asian Nat Prod Res。 2017 Apr;19(4):314-319。

幸运飞艇整合算法 快乐时时彩 幸运飞艇玩法诀窍 幸运飞艇怎么样 如何看北京pk10选号 网上北京pk10怎么玩 幸运飞艇怎样玩可以赢钱 赌幸运飞艇怎样才会赢 幸运飞艇如何玩才能盈利 幸运飞艇怎么样