神经元自噬在缺血缺氧性脑损伤中的作用

自噬是广泛存在于真核细胞中通过溶酶体机制降解自身成分的一种代谢途径.自噬不仅可通过激活经典的自噬小体-溶酶体途径,而且还可通过影响凋亡和坏死的发生、发展对细胞死亡进行调控.目前,自噬在急性脑缺血缺氧后神经元损伤方面的作用及其具体机制尚不明确.研究表明,缺血缺氧后的自噬具有神经保护作用,如维持神经元稳态、减少神经元死亡等;但也有研究认为,自噬能通过激活多种通路加重缺血缺氧后神经元损伤,甚至诱导神经元死亡.

The role of neuronal autophagy in hypoxic-ischemic brain injiny

Autophagy is a metabolic pathway that widely presents in eukaryotic cells through the lysosomal mechanism to degrade its components. Autophagy regulates cell death not only by activating classic autophagosomal-lysosomal pathway, but also by influencing the occurrence and development of apoptosis and necrosis. Currently, the effect of autophagy in neuronal injury after acute cerebral ischemia/hypoxia and its specific mechanisms remain unclear. Studies have demonstrated that the autophagy after ischemia/hypoxia has a neuroprotective effect, such as maintaining neuronal homeostasis and reducing neuronal death; but other studies have also suggested that autophagy may aggravate neuronal injury after ischemia/hypoxia by activating multiple pathways, and even induce neuronal death.