FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2023373493> ?p ?o ?g. }

• W2023373493 endingPage "241" @default.
• W2023373493 startingPage "222" @default.
• W2023373493 abstract "Oxidative stress in the cardiovascular system, including brain microvessels and/or parenchymal cells results in an accumulation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) compounds thus promoting leukocyte adhesion and increasing endothelial permeability. The resulting chronic injury stimulus results in progressive cellular hypometabolism. We propose that hypometabolism, coupled with oxidative stressors, is responsible for most Alzheimer disease (AD) and cerebrovascular accidents (CVAs) and appears to be a central initiating factor for vascular abnormalities, mitochondrial damage and an imbalance in the activity of vasoactive substances, such as different isoforms of nitric oxide synthase (NOS), endothelin-1 (ET-1), oxidative stress markers, mtDNA and mitochondrial enzymes in the vascular wall and in brain parenchymal cells. At higher concentrations, ROS induces cell injury and death, which occurs during the aging process, where accelerated generation of ROS and a gradual decline in cellular antioxidant defense mechanisms, especially in the mitochondria. Vascular endothelial and neuronal mitochondria are especially vulnerable to oxidative stress due to their role in energy supply and use, which can cause a cascade of debilitating factors such as the production of giant and/or vulnerable young mitochondrion who's DNA has been compromised. Therefore, mitochondrial DNA abnormalities such as overproliferation and or deletion can be used as a key marker for diseases differentiation and effectiveness of the treatment. We speculate that specific antioxidants such as acetyl-L-carnitine and R-alpha lipoic acid seem to be potential treatments for AD. They target the factors that damage mitochondria and reverse its effect, thus eliminating the imbalance seen in energy production and restore the normal cellular function, making these antioxidants very powerful alternate strategies for the treatment of cardiovascular cerebrovascular as well as neurodegenerative diseases including AD. Future potential exploration using mtDNA markers can be considered more accurate hallmarks for diagnosis and monitoring treatment of human diseases. The present article discusses some of the patents regarding the oxidative stress." @default.
• W2023373493 created "2016-06-24" @default.
• W2023373493 creator A5004443450 @default.
• W2023373493 creator A5012987732 @default.
• W2023373493 creator A5059674814 @default.
• W2023373493 creator A5064842058 @default.
• W2023373493 date "2011-09-01" @default.
• W2023373493 modified "2023-09-24" @default.
• W2023373493 title "Oxidative Stress Induced Mitochondrial DNA Deletion as a Hallmark forthe Drug Development in the Context of the Cerebrovascular Diseases" @default.
• W2023373493 cites W119165056 @default.
• W2023373493 cites W1228775382 @default.
• W2023373493 cites W1430026677 @default.
• W2023373493 cites W145905393 @default.
• W2023373493 cites W146241754 @default.
• W2023373493 cites W1500094754 @default.
• W2023373493 cites W1505503094 @default.
• W2023373493 cites W1525061277 @default.
• W2023373493 cites W1535816350 @default.
• W2023373493 cites W1542215809 @default.
• W2023373493 cites W1544480566 @default.
• W2023373493 cites W1549308915 @default.
• W2023373493 cites W1610854935 @default.
• W2023373493 cites W1643525023 @default.
• W2023373493 cites W1662308449 @default.
• W2023373493 cites W1694583824 @default.
• W2023373493 cites W1771725737 @default.
• W2023373493 cites W1791996532 @default.
• W2023373493 cites W1883906051 @default.
• W2023373493 cites W1896970469 @default.
• W2023373493 cites W1929009802 @default.
• W2023373493 cites W1966729915 @default.
• W2023373493 cites W1967131207 @default.
• W2023373493 cites W1967237003 @default.
• W2023373493 cites W1971146938 @default.
• W2023373493 cites W1972155682 @default.
• W2023373493 cites W1972863264 @default.
• W2023373493 cites W1973309797 @default.
• W2023373493 cites W1973741828 @default.
• W2023373493 cites W1974297683 @default.
• W2023373493 cites W1976541189 @default.
• W2023373493 cites W1977232394 @default.
• W2023373493 cites W1978348298 @default.
• W2023373493 cites W1979243823 @default.
• W2023373493 cites W1979361284 @default.
• W2023373493 cites W1981779207 @default.
• W2023373493 cites W1981913671 @default.
• W2023373493 cites W1983789627 @default.
• W2023373493 cites W1984964878 @default.
• W2023373493 cites W1985221375 @default.
• W2023373493 cites W1985348492 @default.
• W2023373493 cites W1985786980 @default.
• W2023373493 cites W1986950646 @default.
• W2023373493 cites W1988627939 @default.
• W2023373493 cites W1988726352 @default.
• W2023373493 cites W1990195300 @default.
• W2023373493 cites W1992602428 @default.
• W2023373493 cites W1993775827 @default.
• W2023373493 cites W1994093790 @default.
• W2023373493 cites W1994503827 @default.
• W2023373493 cites W1995379325 @default.
• W2023373493 cites W1996537516 @default.
• W2023373493 cites W1997776892 @default.
• W2023373493 cites W2000468913 @default.
• W2023373493 cites W2002219115 @default.
• W2023373493 cites W2002669267 @default.
• W2023373493 cites W2002957102 @default.
• W2023373493 cites W2004526436 @default.
• W2023373493 cites W2008481928 @default.
• W2023373493 cites W2010224794 @default.
• W2023373493 cites W2010251102 @default.
• W2023373493 cites W2010754688 @default.
• W2023373493 cites W2012786488 @default.
• W2023373493 cites W2015148186 @default.
• W2023373493 cites W2016293448 @default.
• W2023373493 cites W2016422645 @default.
• W2023373493 cites W2018098602 @default.
• W2023373493 cites W2018692335 @default.
• W2023373493 cites W2020068741 @default.
• W2023373493 cites W2020138738 @default.
• W2023373493 cites W2020914812 @default.
• W2023373493 cites W2022699060 @default.
• W2023373493 cites W2024022041 @default.
• W2023373493 cites W2025300385 @default.
• W2023373493 cites W2027189256 @default.
• W2023373493 cites W2028676745 @default.
• W2023373493 cites W2029094496 @default.
• W2023373493 cites W2029106340 @default.
• W2023373493 cites W2030142800 @default.
• W2023373493 cites W2030159889 @default.
• W2023373493 cites W2031738386 @default.
• W2023373493 cites W2032350023 @default.
• W2023373493 cites W2032769405 @default.
• W2023373493 cites W2033496106 @default.
• W2023373493 cites W2037500564 @default.
• W2023373493 cites W2037542399 @default.
• W2023373493 cites W2038785443 @default.
• W2023373493 cites W2042094492 @default.
• W2023373493 cites W2043093287 @default.

• next