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- W2779711828 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." @default.
- W2779711828 created "2018-01-05" @default.
- W2779711828 creator A5020738242 @default.
- W2779711828 creator A5069771802 @default.
- W2779711828 date "2017-01-01" @default.
- W2779711828 modified "2023-10-05" @default.
- W2779711828 title "Mitochondrial Dysfunction in Ischemic Stroke" @default.
- W2779711828 cites W1483486462 @default.
- W2779711828 cites W1485627882 @default.
- W2779711828 cites W1502551831 @default.
- W2779711828 cites W1514967918 @default.
- W2779711828 cites W1518138852 @default.
- W2779711828 cites W1635047156 @default.
- W2779711828 cites W1705639264 @default.
- W2779711828 cites W1796740069 @default.
- W2779711828 cites W1858063084 @default.
- W2779711828 cites W1881066497 @default.
- W2779711828 cites W1909216755 @default.
- W2779711828 cites W1933759996 @default.
- W2779711828 cites W1935432045 @default.
- W2779711828 cites W1963548069 @default.
- W2779711828 cites W1967268953 @default.
- W2779711828 cites W1968351069 @default.
- W2779711828 cites W1968709066 @default.
- W2779711828 cites W1969004566 @default.
- W2779711828 cites W1969849548 @default.
- W2779711828 cites W1974614961 @default.
- W2779711828 cites W1974911740 @default.
- W2779711828 cites W1977202835 @default.
- W2779711828 cites W1977258127 @default.
- W2779711828 cites W1980829692 @default.
- W2779711828 cites W1984256496 @default.
- W2779711828 cites W1984420703 @default.
- W2779711828 cites W1985796485 @default.
- W2779711828 cites W1987471587 @default.
- W2779711828 cites W1990506628 @default.
- W2779711828 cites W1993149192 @default.
- W2779711828 cites W1995195218 @default.
- W2779711828 cites W1996308628 @default.
- W2779711828 cites W1997801295 @default.
- W2779711828 cites W1998328762 @default.
- W2779711828 cites W2001544013 @default.
- W2779711828 cites W2004595433 @default.
- W2779711828 cites W2007372190 @default.
- W2779711828 cites W2008582431 @default.
- W2779711828 cites W2008841747 @default.
- W2779711828 cites W2008939548 @default.
- W2779711828 cites W2010422175 @default.
- W2779711828 cites W2011176180 @default.
- W2779711828 cites W2012103983 @default.
- W2779711828 cites W2016597337 @default.
- W2779711828 cites W2017431540 @default.
- W2779711828 cites W2018409191 @default.
- W2779711828 cites W2020722847 @default.
- W2779711828 cites W2022803736 @default.
- W2779711828 cites W2023105087 @default.
- W2779711828 cites W2024902320 @default.
- W2779711828 cites W2025128734 @default.
- W2779711828 cites W2028092741 @default.
- W2779711828 cites W2029241688 @default.
- W2779711828 cites W2032413974 @default.
- W2779711828 cites W2033453669 @default.
- W2779711828 cites W2035420440 @default.
- W2779711828 cites W2036411709 @default.
- W2779711828 cites W2042515284 @default.
- W2779711828 cites W2045840821 @default.
- W2779711828 cites W2048194799 @default.
- W2779711828 cites W2049114235 @default.
- W2779711828 cites W2049378335 @default.
- W2779711828 cites W2051029351 @default.
- W2779711828 cites W2054120161 @default.
- W2779711828 cites W2060507522 @default.
- W2779711828 cites W2062853648 @default.
- W2779711828 cites W2063669247 @default.
- W2779711828 cites W2063744637 @default.
- W2779711828 cites W2064598952 @default.
- W2779711828 cites W2071893373 @default.
- W2779711828 cites W2079822311 @default.
- W2779711828 cites W2082259697 @default.
- W2779711828 cites W2086764184 @default.
- W2779711828 cites W2087350238 @default.
- W2779711828 cites W2089272650 @default.
- W2779711828 cites W2090217381 @default.
- W2779711828 cites W2105754268 @default.
- W2779711828 cites W2111857492 @default.
- W2779711828 cites W2118397007 @default.
- W2779711828 cites W2119159602 @default.
- W2779711828 cites W2119683782 @default.
- W2779711828 cites W2122827315 @default.
- W2779711828 cites W2127876602 @default.
- W2779711828 cites W2128268504 @default.
- W2779711828 cites W2128557475 @default.
- W2779711828 cites W2135725455 @default.
- W2779711828 cites W2140751228 @default.
- W2779711828 cites W2146733063 @default.
- W2779711828 cites W2147597448 @default.
- W2779711828 cites W2149249593 @default.
- W2779711828 cites W2149419595 @default.