Can I get help constructing a concept map for the information provided below? Autophagy has a complex signaling control system, and manystudies have indicated that the PI3K/Akt/mTOR signaling path-way is closely related to autophagy. Downstream phosphorylationof Akt can activate Tuberous Sclerosis 1/2 (TSC1/2), which fur-ther promotes mTOR activation. mTOR functions by inhibitingthe downstream molecular complex ULK1 to negatively regulateautophagy levels [9,10]. However, mTOR activity is inhibited inthe absence of nutrients and activates autophagy; in contrast,autophagy is inhibited when mTOR is activated in the presenceof excess nutrients [11,12]. Noshita N found that p-Akt expres-sion decreased 1h after injury in a study of traumatic braininjury (TBI) and continued to decrease for 4h. p-Akt expressionwas increased after TBI in the hippocampal CA1 region, and fur-ther studies showed that p-Akt plays a protective role after TBI[13].Mitochondria are the control centers of apoptosis and playa decisive role in the occurrence of apoptosis after the cell isaffected by adverse external factors [14]. Cytochrome C is thekey signaling molecule in the mitochondrial apoptosis pathway.Release of cytochrome C from the mitochondria can activate theapoptotic effector caspase-3, leading to apoptosis, while caspase-3activation can in turn promote the release of cytochrome C fromthe mitochondria, leading to a vicious cycle [15,16]. The earlystage of rapamycin-induced brain injury can be reduced, mainlythrough the enhancement of autophagy, which reduces mitochon-drial cytochrome Crelease [17]. Current research has demonstratedthat beclin-1 can function as a caspase target; the product can alterhow mitochondrial membrane permeability promotes cell apopto-sis, indicating a molecular link between autophagy and apoptosis[18–20]. However, the relationship between autophagy and apo-ptosis in spinal cord injury is unclear. In this study, we used anin vitro mechanical injury spinal cord neural cell model to evaluatethe relationship between autophagy signal transduction and themitochondrial apoptotic pathway. 1. Introductioninjury have become an intensely researched topic. Autophagy isa protective physiological process in eukaryotic organisms that ischaracterized by the formation of a bilayer membrane structureand is associated with abnormal proteins and damaged organellesin the cytoplasm[4-6]. Kanno H found that the autophagy-specificprotein microtubule-associated protein 1 light chain 3 (LC3) washighly expressed in injured spinal cord neurons, which confirmedthe existence of autophagy in neuronal cells [7]. By establishing anin vitro model of spinal cord injury, we found that autophagy canbe induced in the early stage of injury. Further study revealed thatautophagy was enhanced after injury, which could reduce the levelof apoptosis and protect neurons [8].Spinal cord injury is a serious neurological disorder. The sec-ondary pathological changes induced by spinal cord injury are thegreatest obstacle to repair; these changes include edema, necro-sis, apoptosis, oxidative stress, inflammation and other processes[1-3]. Therefore, the neural functions associated with spinal cord* Corresponding author.E-mail address: 13705977551@163.com (W. Liu).1 Joint first authors.http://dx.doi.org/10.1016/j.neulet.2017.07.0360304-3940/© 2017 Published by Elsevier Ireland Ltd.

Question

Accepted Answer

Structure and Function of Mitochondria
Mitochondria structure is quite compact, and all of its…