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    • Stroke also known as a

    2024-02-02

    Stroke, also known as a cerebrovascular accident or Phosphatase Inhibitor Cocktail 1 (100X in DMSO) attack, is one of the leading causes of death and disability worldwide (Haley et al., 2017; Hankey, 2017; Lie et al., 2017). According to the data released by the World Health Organization (WHO), stroke occurs every 5 s worldwide (WHO, 2016). Every year, there are about 15 million people suffered from brain injury followed by stroke (WHO, 2016). Of these, more than 5 million die and another 5 million are left permanently or temporarily disabled, causing a heavy economic burden on family and community (WHO, 2016). The burden of stroke and stroke-related diseases is rather great. The data from WHO showed that the burden of stroke may rise from around 38 million disability-adjusted life years (DALYs) in 1990 to 61 million DALYs in 2020 globally (WHO, 2016). Many factors contribute to the onset and development of ischemic stroke. Although great efforts have been made to improve the understanding of ischemic stroke, there remain unanswered questions. Over the past two decades, accumulating evidence has demonstrated that autophagy is extensively involved in ischemic stroke. However, the exact role and molecular mechanisms of autophagy process in ischemic stroke are not fully elucidated. In this review, we will provide a comprehensive overview of the advance in this exciting research field.
    Autophagy process and signaling in normal condition and ischemic stroke
    Roles of autophagy in ischemic stroke The normal functions of brain require sufficient oxygen and nutrition via the blood supply. The oxygen and nutrition can be fluently transported across the blood-brain barrier and absorbed by the brain tissues for energy generation and application. Generally, stroke can be sub-classified into two types: ischemic stroke, due to blockade of cerebral artery and lack of blood flow perfusion, and hemorrhagic stroke, a non-traumatic intracranial hemorrhage. Ischemic stroke accounts for about 87% in the total stroke cases. When the blood flow is substantially decreased or completely blocked by a clot or other dissolvable obstruction, ischemic stroke occurs. Biochemically, there is a profound reduction in intracellular adenosine 5′-triphosphate (ATP) level for very short periods during ischemia, possibly for less than 1 min. If the blood flow is blocked for more than a few seconds, brain cell starts to response this challenge due to the lack of oxygen. If the ischemic time is prolonged to minutes, the vulnerable brain cells in the ischemic core area start to die and a permanent neural damage is subsequently caused (Moskowitz et al., 2010; Wang et al., 2017; Yu et al., 2017). As we discussed previously, autophagy process is closely involved in the pathogenesis and progression of ischemic stroke. The current understanding on the impact of autophagy on ischemic stroke will be presented and discussed in the following contents.
    Autophagy in neuroprotection of ischemic preconditioning, perconditioning and postconditioning Ischemic preconditioning is a phenomenon that challenging an organ with brief episodes of ischemic insult beforehand is able to protect against the subsequent prolonged and lethal ischemic injury. While the conditioning stimulus is applied during or after (reperfusion phase) the ischemic event, they are called ischemic perconditioning and postconditioning, respectively. Most of organs, including brain, heart, liver and kidney, would benefit from ischemic preconditioning, perconditioning and postconditioning (Kloner, 2009; Liu et al., 2016c; Pierce et al., 2017; Sheng and Qin, 2015; Zhao, 2007). The molecular mechanisms are not fully understood. The inhibitory effects of ischemic preconditioning, preconditioning and postconditioning on oxidative stress activation, mitochondrial derangement and apoptosis activation are reported to be involved. In recent years, several lines of evidence have converged to support the idea that the moderate autophagy might be a crucial mediator of the protection of ischemic preconditioning, preconditioning and postconditioning.