FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4384523905> ?p ?o ?g. }

• W4384523905 endingPage "44" @default.
• W4384523905 startingPage "25" @default.
• W4384523905 abstract "Oxidative stress is a major contributor to ischaemia reperfusion injurymediated myocardial infarction. Coronary ischemia deprives the heart muscles of nutrients and oxygen in the areas away from the site of arterial blockage, rendering cardiomyocytes unable to utilise aerobic metabolism to support their energy requirements. Homeostatic intracellular signalling systems, such as the hypoxiainducible factor (HIF) transcription factor cascade, sense the low oxygen environment. This in turn stimulates the upregulation of numerous compensatory mechanisms which are ultimately involved in elevating anaerobic glycolysis and promoting angiogenesis and vascularization. The increased anaerobic metabolism increases the production of lactic acid hence metabolic acidosis. This leads to myocyte death and the expansion of the size of the original area of the infarct. Under normal aerobic conditions, the myocardium generally metabolises relatively high levels of adenosine triphosphates (ATP). In contrast, during ischemia, the shift in energy production to glycolysis results in the inefficient production of ATP and constitutes a pathological feature, and if not reversed early, it may lead to complications such as heart failure and ischemia-induced atrial or ventricular fibrillation. Despite the widespread use of fibrinolytic agents and new types of angioplasty procedures for the treatment of myocardial infarction, often new sets of complications persist. These include the occurrence of extensive tissue injury caused by myocardial reperfusion through the reintroduction of oxygen to the previous ischemic tissues because of the excessive generation of reactive oxygen species (ROSs) and depletion of antioxidants. Widespread production of ROS damages the plasma membrane and stimulates the release of various proinflammatory agents. Several proteins become denatured for example receptors, ionic channels, transporters, or components of transduction pathways through oxidation by ROS. Altered protein structure inhibits their functions leading to the disruption of vital cellular processes. The onset of reperfusion injury is further exacerbated by the activation and infiltration of the infarcted area by polymorphonuclear leukocytes (PMNs). Several studies have identified the release of different leukocyte intracellular factors during PMN activation such as selectins and b2-integrins to be related to the magnitude of tissue damage. Some studies have shown that antagonists for leukocytes intracellular factors such as selectins abrogate PMN activation and reduce the infarct size.More recent publications have shown that PMN activation is closely linked to the activation of other cells involved in the inflammatory response. For example, during myocardial ischemia–reperfusion injury, it has been shown that the activity of neutrophils is also modulated by lymphocytes and macrophages. This chapter summarises the interaction between oxidative stress, activation of different leukocytes and the release of factors involved in the generation of reperfusion injury." @default.
• W4384523905 created "2023-07-18" @default.
• W4384523905 creator A5038771290 @default.
• W4384523905 creator A5073758619 @default.
• W4384523905 date "2023-07-16" @default.
• W4384523905 modified "2023-09-27" @default.
• W4384523905 title "Oxidative Stress and Leukocytes Activation - The Two Keystones of Ischemia/Reperfusion Injury during Myocardial Infarction, Valve Disease, and Atrial Fibrillation" @default.
• W4384523905 cites W1487373628 @default.
• W4384523905 cites W1499297460 @default.
• W4384523905 cites W1504373474 @default.
• W4384523905 cites W1653408396 @default.
• W4384523905 cites W1849785625 @default.
• W4384523905 cites W1909981107 @default.
• W4384523905 cites W1964257639 @default.
• W4384523905 cites W1966114904 @default.
• W4384523905 cites W1966558949 @default.
• W4384523905 cites W1968353658 @default.
• W4384523905 cites W1971321175 @default.
• W4384523905 cites W1976616659 @default.
• W4384523905 cites W1984602022 @default.
• W4384523905 cites W1984996259 @default.
• W4384523905 cites W1988449390 @default.
• W4384523905 cites W1990163699 @default.
• W4384523905 cites W1990840232 @default.
• W4384523905 cites W1994456301 @default.
• W4384523905 cites W1995461730 @default.
• W4384523905 cites W1999033829 @default.
• W4384523905 cites W2002420195 @default.
• W4384523905 cites W2002808246 @default.
• W4384523905 cites W2003213503 @default.
• W4384523905 cites W2005175065 @default.
• W4384523905 cites W2009804037 @default.
• W4384523905 cites W2018702692 @default.
• W4384523905 cites W2019438826 @default.
• W4384523905 cites W2025782661 @default.
• W4384523905 cites W2026464064 @default.
• W4384523905 cites W2029965951 @default.
• W4384523905 cites W2042662902 @default.
• W4384523905 cites W2043427064 @default.
• W4384523905 cites W2051329265 @default.
• W4384523905 cites W2065634680 @default.
• W4384523905 cites W2066963386 @default.
• W4384523905 cites W2075956511 @default.
• W4384523905 cites W2078003859 @default.
• W4384523905 cites W2081068301 @default.
• W4384523905 cites W2084449053 @default.
• W4384523905 cites W2084500917 @default.
• W4384523905 cites W2087774615 @default.
• W4384523905 cites W2088820548 @default.
• W4384523905 cites W2088955890 @default.
• W4384523905 cites W2090500320 @default.
• W4384523905 cites W2093391702 @default.
• W4384523905 cites W2097236746 @default.
• W4384523905 cites W2099273954 @default.
• W4384523905 cites W2099675490 @default.
• W4384523905 cites W2106824469 @default.
• W4384523905 cites W2109040278 @default.
• W4384523905 cites W2109698138 @default.
• W4384523905 cites W2112821970 @default.
• W4384523905 cites W2113495231 @default.
• W4384523905 cites W2113871285 @default.
• W4384523905 cites W2115708356 @default.
• W4384523905 cites W2115992753 @default.
• W4384523905 cites W2124154927 @default.
• W4384523905 cites W2133933535 @default.
• W4384523905 cites W2137363665 @default.
• W4384523905 cites W2146190354 @default.
• W4384523905 cites W2151788147 @default.
• W4384523905 cites W2155121555 @default.
• W4384523905 cites W2165203443 @default.
• W4384523905 cites W2180741588 @default.
• W4384523905 cites W2253973659 @default.
• W4384523905 cites W2308516605 @default.
• W4384523905 cites W2590815007 @default.
• W4384523905 cites W2645682151 @default.
• W4384523905 cites W2733405828 @default.
• W4384523905 cites W2741602250 @default.
• W4384523905 cites W2755850443 @default.
• W4384523905 cites W2763106122 @default.
• W4384523905 cites W2765456583 @default.
• W4384523905 cites W2791064861 @default.
• W4384523905 cites W2793594895 @default.
• W4384523905 cites W2884858612 @default.
• W4384523905 cites W2922049651 @default.
• W4384523905 cites W2971456522 @default.
• W4384523905 cites W2980918374 @default.
• W4384523905 cites W3103025920 @default.
• W4384523905 cites W3175048990 @default.
• W4384523905 cites W4210982394 @default.
• W4384523905 cites W4247106487 @default.
• W4384523905 cites W97712012 @default.
• W4384523905 doi "https://doi.org/10.2174/9789815165012123010005" @default.
• W4384523905 hasPublicationYear "2023" @default.
• W4384523905 type Work @default.
• W4384523905 citedByCount "0" @default.
• W4384523905 crossrefType "book-chapter" @default.
• W4384523905 hasAuthorship W4384523905A5038771290 @default.
• W4384523905 hasAuthorship W4384523905A5073758619 @default.

• next