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• W2016178459 abstract "Cerebral ischemia leads to a massive increase in cytoplasmic calcium activity resulting from an influx of calcium ions into cells and a release of calcium from mitochondria and endoplasmic reticulum (ER). It is widely believed that this increase in cytoplasmic calcium activity plays a major role in ischemic cell injury in neurons. Recently, this concept was modified, taking into account that disturbances occurring during ischemia are potentially reversible: it then was proposed that after reversible ischemia, calcium ions are taken up by mitochondria, leading to disturbances of oxidative phosphorylation, formation of free radicals, and deterioration of mitochondrial functions. The current review focuses on the possible role of disturbances of ER calcium homeostasis in the pathologic process culminating in ischemic cell injury. The ER is a subcellular compartment that fulfills important functions such as the folding and processing of proteins, all of which are strictly calcium dependent. ER calcium activity is therefore relatively high, lying in the lower millimolar range (i.e., close to that of the extracellular space). Depletion of ER calcium stores is a severe form of stress to which cells react with a highly conserved stress response, the most important changes being a suppression of global protein synthesis and activation of stress gene expression. The response of cells to disturbances of ER calcium homeostasis is almost identical to their response to transient ischemia, implying common underlying mechanisms. Many observations from experimental studies indicate that disturbances of ER calcium homeostasis are involved in the pathologic process leading to ischemic cell injury. Evidence also has been presented that depletion of ER calcium stores alone is sufficient to activate the process of programmed cell death. Furthermore, it has been shown that activation of the ER-resident stress response system by a sublethal form of stress affords tolerance to other, potentially lethal insults. Also, disturbances of ER function have been implicated in the development of degenerative disorders such as prion disease and Alzheimer's disease. Thus, disturbances of the functioning of the ER may be a common denominator of neuronal cell injury in a wide variety of acute and chronic pathologic states of the brain. Finally, there is evidence that ER calcium homeostasis plays a key role in maintaining cells in their physiologic state, since depletion of ER calcium stores causes growth arrest and cell death, whereas cells in which the regulatory link between ER calcium homeostasis and protein synthesis has been blocked enter a state of uncontrolled proliferation." @default.
• W2016178459 created "2016-06-24" @default.
• W2016178459 creator A5039283168 @default.
• W2016178459 creator A5077936053 @default.
• W2016178459 date "1999-01-01" @default.
• W2016178459 modified "2023-09-27" @default.
• W2016178459 title "Disturbances of the Functioning of Endoplasmic Reticulum: A Key Mechanism Underlying Neuronal Cell Injury?" @default.
• W2016178459 cites W1032278008 @default.
• W2016178459 cites W105324358 @default.
• W2016178459 cites W1483200187 @default.
• W2016178459 cites W1496939314 @default.
• W2016178459 cites W1522731616 @default.
• W2016178459 cites W1525421301 @default.
• W2016178459 cites W1535214827 @default.
• W2016178459 cites W1535365166 @default.
• W2016178459 cites W1536352052 @default.
• W2016178459 cites W1538657525 @default.
• W2016178459 cites W1548027699 @default.
• W2016178459 cites W1549105044 @default.
• W2016178459 cites W1549546756 @default.
• W2016178459 cites W1563280839 @default.
• W2016178459 cites W1569469862 @default.
• W2016178459 cites W1605456662 @default.
• W2016178459 cites W1608735237 @default.
• W2016178459 cites W1639005451 @default.
• W2016178459 cites W1776522267 @default.
• W2016178459 cites W1820758986 @default.
• W2016178459 cites W1859293501 @default.
• W2016178459 cites W191500074 @default.
• W2016178459 cites W1915631065 @default.
• W2016178459 cites W1963764076 @default.
• W2016178459 cites W1965744968 @default.
• W2016178459 cites W1967057358 @default.
• W2016178459 cites W1967824319 @default.
• W2016178459 cites W1968620302 @default.
• W2016178459 cites W1969072862 @default.
• W2016178459 cites W1969612832 @default.
• W2016178459 cites W1970053452 @default.
• W2016178459 cites W1970812281 @default.
• W2016178459 cites W1972681977 @default.
• W2016178459 cites W1973869611 @default.
• W2016178459 cites W1974887294 @default.
• W2016178459 cites W1974892577 @default.
• W2016178459 cites W1975896299 @default.
• W2016178459 cites W1976505704 @default.
• W2016178459 cites W1979768246 @default.
• W2016178459 cites W1979773315 @default.
• W2016178459 cites W1979785053 @default.
• W2016178459 cites W1980011256 @default.
• W2016178459 cites W1980572916 @default.
• W2016178459 cites W1981070246 @default.
• W2016178459 cites W1986228861 @default.
• W2016178459 cites W1988406918 @default.
• W2016178459 cites W1991542726 @default.
• W2016178459 cites W1993025892 @default.
• W2016178459 cites W1994671755 @default.
• W2016178459 cites W1994733478 @default.
• W2016178459 cites W1995175521 @default.
• W2016178459 cites W1995684052 @default.
• W2016178459 cites W1997778815 @default.
• W2016178459 cites W1997901402 @default.
• W2016178459 cites W1998595310 @default.
• W2016178459 cites W2001068917 @default.
• W2016178459 cites W2002744696 @default.
• W2016178459 cites W2003282272 @default.
• W2016178459 cites W2004540956 @default.
• W2016178459 cites W2005666794 @default.
• W2016178459 cites W2007470466 @default.
• W2016178459 cites W2008203066 @default.
• W2016178459 cites W2008524988 @default.
• W2016178459 cites W2010682324 @default.
• W2016178459 cites W2013310858 @default.
• W2016178459 cites W2014470707 @default.
• W2016178459 cites W2015556894 @default.
• W2016178459 cites W2016716112 @default.
• W2016178459 cites W2016933143 @default.
• W2016178459 cites W2017583591 @default.
• W2016178459 cites W2018554539 @default.
• W2016178459 cites W2020258831 @default.
• W2016178459 cites W2020622209 @default.
• W2016178459 cites W2021567222 @default.
• W2016178459 cites W2022137499 @default.
• W2016178459 cites W2024167379 @default.
• W2016178459 cites W2024179907 @default.
• W2016178459 cites W2024773521 @default.
• W2016178459 cites W2024856889 @default.
• W2016178459 cites W2024944868 @default.
• W2016178459 cites W2025005459 @default.
• W2016178459 cites W2025818427 @default.
• W2016178459 cites W2026728451 @default.
• W2016178459 cites W2026740383 @default.
• W2016178459 cites W2028286425 @default.
• W2016178459 cites W2029205666 @default.
• W2016178459 cites W2029738794 @default.
• W2016178459 cites W2031688775 @default.
• W2016178459 cites W2032221839 @default.
• W2016178459 cites W2032575416 @default.
• W2016178459 cites W2033828028 @default.

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