Mitochondrial Dysfunction in Ischemic Stroke

A description of the problem but NO solution. Damn, I hate these lazy researchers. Do stroke survivors care about describing their problems? NO!!!. Provide solutions to their problems you blithering idiots. 
https://link.springer.com/chapter/10.1007/978-981-10-5804-2_10

• Authors
• Authors and affiliations

• Qiang LiEmail author
• Shane Gao

• Qiang Li
  • 1
  Email author
• Shane Gao
  • 2

1. 1.Department of NeurologyShanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of MedicineShanghaiChina
2. 2.East HospitalTongji University School of MedicineShanghaiChina

Chapter

First Online: 22 December 2017

• 15 Downloads

Part of the Translational Medicine Research book series (TRAMERE)

Abstract

Mitochondrion is the powerhouse of the cell, which is essential for cell survival after cerebral ischemia/reperfusion. Mitochondrion is a sensitive organelle susceptible to brain ischemia/reperfusion injury. Mitochondrial dysfunction is one of the foremost events involved in brain ischemia/reperfusion process and then induces further damage to brain cells. It influences not only the fate of neural cells but also blood-brain barrier permeability after ischemic stroke. The underlying mechanism of mitochondria dysfunction in determining cell survival and cell death involves in many cell signaling pathways including apoptosis, autophagy, and mitochondrial biogenesis. Mitochondria apoptosis pathway was extensively explored in the past. Many apoptosis-related regulator families were involved in mitochondria apoptosis pathway, like Bcl-2 family, caspase family, p53 gene family, and so on. On the other hand, ROS injury, Ca²⁺ overload, and mPTP opening are also detrimental to mitochondrial function after cerebral ischemia/reperfusion. Recent interests were focused on the important role of mitophagy and mitochondrial biogenesis on cell survival after cerebral ischemia/reperfusion, which are thought to be endogenous protective mechanisms of mitochondrial dysfunction. Therefore, under ischemia/reperfusion conditions, promoting endogenous protective mechanisms and inhibiting exogenous damage mechanisms are both important therapeutic strategies. In summary, mitochondrial dysfunction is not simply the result of ischemia/reperfusion injury but also the cause of cascading damage. So, protecting dysfunctional mitochondria is pivotal to cell survival after ischemic stroke.