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- W2895587672 abstract "Neurodegenerative diseases, such as Alzheimer's and Parkinson's disease share common cell death mechanisms despite significant differences in the underlying pathology causing neuronal dysfunction and death. Current treatments for these diseases are merely symptomatic and clearly limited, as they do not slow down the progression of neurodegeneration. Therefore, it is of the utmost importance to reveal the mechanisms of neuronal cell death in order to identify novel targets for effective causal therapies. In this book chapter we summarize current knowledge on the molecular mechanisms underlying oxytosis, a particular mode of regulated cell death induced by oxidative stress. In oxytosis, inhibition of the glutamate/cysteine (Xc− Cys/Glu) antiporter, depletion of glutathione (GSH), activation of 12/15 lipoxygenases (LOX), and formation of reactive oxygen species (ROS) are pivotal up-stream mechanisms of mitochondrial dysfunction. Further intracellular signaling pathways linked to oxytosis include mitogen-activated protein kinases (MAPKs), a family of serine/threonine protein kinases consisting of growth factor-regulated extracellular signal-related kinases (ERKs), stress-activated c-Jun NH2-terminal kinases (JNKs) and p38 MAPKs. Mitochondria are regarded as the key decision points in oxytosis, where mitochondrial fragmentation (fission, activation of DRP1, BID and BAX) and accelerated mitochondrial ROS formation determine the final phase of cell death. Downstream mechanisms of mitochondrial dysfunction include the disruption of mitochondrial membrane integrity and the release of pro-apoptotic factors such as apoptosis inducing factor (AIF). In this chapter we address the molecular mechanisms underlying oxytosis with emphasis on mitochondrial and endoplasmic reticulum dependent pathways that could be exposed as potential therapeutic strategies to prevent or rescue neuronal death in neurodegenerative diseases." @default.
- W2895587672 created "2018-10-12" @default.
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- W2895587672 date "2018-09-12" @default.
- W2895587672 modified "2023-09-27" @default.
- W2895587672 title "Molecular Mechanisms Underlying Oxytosis" @default.
- W2895587672 cites W1486333767 @default.
- W2895587672 cites W1517407659 @default.
- W2895587672 cites W1521411817 @default.
- W2895587672 cites W1523726718 @default.
- W2895587672 cites W1525431558 @default.
- W2895587672 cites W1528634994 @default.
- W2895587672 cites W1529774113 @default.
- W2895587672 cites W1562623205 @default.
- W2895587672 cites W1769202563 @default.
- W2895587672 cites W1963844828 @default.
- W2895587672 cites W1965512256 @default.
- W2895587672 cites W1966067605 @default.
- W2895587672 cites W1966779294 @default.
- W2895587672 cites W1967811402 @default.
- W2895587672 cites W1968055572 @default.
- W2895587672 cites W1968439134 @default.
- W2895587672 cites W1970090817 @default.
- W2895587672 cites W1970248089 @default.
- W2895587672 cites W1971391716 @default.
- W2895587672 cites W1972331889 @default.
- W2895587672 cites W1973080574 @default.
- W2895587672 cites W1973290614 @default.
- W2895587672 cites W1973966118 @default.
- W2895587672 cites W1974575580 @default.
- W2895587672 cites W1974980101 @default.
- W2895587672 cites W1976349741 @default.
- W2895587672 cites W1976779549 @default.
- W2895587672 cites W1977258127 @default.
- W2895587672 cites W1980100638 @default.
- W2895587672 cites W1981759131 @default.
- W2895587672 cites W1983863419 @default.
- W2895587672 cites W1984035373 @default.
- W2895587672 cites W1985012493 @default.
- W2895587672 cites W1985235409 @default.
- W2895587672 cites W1985951335 @default.
- W2895587672 cites W1986568749 @default.
- W2895587672 cites W1988264669 @default.
- W2895587672 cites W1989053288 @default.
- W2895587672 cites W1989272348 @default.
- W2895587672 cites W1989347991 @default.
- W2895587672 cites W1991958238 @default.
- W2895587672 cites W1994525399 @default.
- W2895587672 cites W1995805913 @default.
- W2895587672 cites W1995986855 @default.
- W2895587672 cites W1997898002 @default.
- W2895587672 cites W1998994319 @default.
- W2895587672 cites W2000083423 @default.
- W2895587672 cites W2001291607 @default.
- W2895587672 cites W2005788760 @default.
- W2895587672 cites W2007636933 @default.
- W2895587672 cites W2007794772 @default.
- W2895587672 cites W2009003493 @default.
- W2895587672 cites W2011492248 @default.
- W2895587672 cites W2012645913 @default.
- W2895587672 cites W2013310858 @default.
- W2895587672 cites W2014202579 @default.
- W2895587672 cites W2014364385 @default.
- W2895587672 cites W2014999693 @default.
- W2895587672 cites W2016293448 @default.
- W2895587672 cites W2018692481 @default.
- W2895587672 cites W2021693564 @default.
- W2895587672 cites W2023542615 @default.
- W2895587672 cites W2025251808 @default.
- W2895587672 cites W2026035029 @default.
- W2895587672 cites W2030532419 @default.
- W2895587672 cites W2032413974 @default.
- W2895587672 cites W2032444047 @default.
- W2895587672 cites W2037612957 @default.
- W2895587672 cites W2038920951 @default.
- W2895587672 cites W2039158815 @default.
- W2895587672 cites W2043353183 @default.
- W2895587672 cites W2046378591 @default.
- W2895587672 cites W2047394489 @default.
- W2895587672 cites W2049779036 @default.
- W2895587672 cites W2049876394 @default.
- W2895587672 cites W2050746675 @default.
- W2895587672 cites W2055655639 @default.
- W2895587672 cites W2056015556 @default.
- W2895587672 cites W2056923392 @default.
- W2895587672 cites W2060811345 @default.
- W2895587672 cites W2061876807 @default.
- W2895587672 cites W2062853648 @default.
- W2895587672 cites W2063265691 @default.
- W2895587672 cites W2065084983 @default.
- W2895587672 cites W2068988368 @default.