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• W2765863160 abstract "Thyroid hormones affect growth, development and metabolism of vertebrates, and are considered the main regulators of their homeostasis. On the other hand, elevated circulating levels of thyroid hormones are associated with modifications in the whole organism (weight loss and increased metabolism and temperature) and in several body regions. Indeed, tachycardia, atrial arrhythmias, heart failure, muscle weakness and wasting, bone mass loss, and hepatobiliary complications are commonly found in hyperthyroid animals and humans. Most of the thyroid hormone actions result from influences on transcription of T3-responsive genes, which are mediated through nuclear receptors. However, there is significant evidence for involvement of tissue oxidative stress in some dysfunctions shown in hyperthyroid state. Mitochondria have been thought to both play a major role in tissue oxidative damage and dysfunction and provide protection against excessive tissue dysfunction, through several mechanisms including increased expression of uncoupling proteins, proteolytic enzymes and transcriptional coactivator PGC-1, and stimulated opening of permeability transition pores. Actually, examination of the most recent data confirms that, in hyperthyroid state, mitochondria play a major role in tissue oxidative stress and rescue from excessive dysfunction. However, such data have also shown the substantial interplay between mitochondria and other sources of ROS and the role that, in pathological conditions, such sources play in generating oxidative stress and promoting survival mechanisms, such as autophagy and apoptosis. These observations suggest that cellular ROS producers could provide a significant contribution to processes that, in hyperthyroid state, oxidatively damage tissues and assure their survival. Keywords: Antioxidant defenses, hyperthyroidism, oxidative damage, mitochondria, ros production, ros sources, autophagy, apoptosis." @default.
• W2765863160 created "2017-11-10" @default.
• W2765863160 creator A5059456880 @default.
• W2765863160 creator A5066267860 @default.
• W2765863160 creator A5087006093 @default.
• W2765863160 date "2015-07-10" @default.
• W2765863160 modified "2023-09-27" @default.
• W2765863160 title "Role of Mitochondria and Other ROS Sources in Hyperthyroidism-Linked Oxidative Stress" @default.
• W2765863160 cites W104178420 @default.
• W2765863160 cites W109036740 @default.
• W2765863160 cites W12155457 @default.
• W2765863160 cites W135169020 @default.
• W2765863160 cites W143520015 @default.
• W2765863160 cites W147697280 @default.
• W2765863160 cites W1488165550 @default.
• W2765863160 cites W1492322138 @default.
• W2765863160 cites W1497174676 @default.
• W2765863160 cites W1499834471 @default.
• W2765863160 cites W150646263 @default.
• W2765863160 cites W1509520311 @default.
• W2765863160 cites W1509698999 @default.
• W2765863160 cites W1520534756 @default.
• W2765863160 cites W1524418166 @default.
• W2765863160 cites W1528220495 @default.
• W2765863160 cites W1530972565 @default.
• W2765863160 cites W1532078988 @default.
• W2765863160 cites W1540436551 @default.
• W2765863160 cites W1553877517 @default.
• W2765863160 cites W1557712018 @default.
• W2765863160 cites W1557926042 @default.
• W2765863160 cites W1558113022 @default.
• W2765863160 cites W1559531158 @default.
• W2765863160 cites W1565127991 @default.
• W2765863160 cites W1579774371 @default.
• W2765863160 cites W1586099293 @default.
• W2765863160 cites W1597717523 @default.
• W2765863160 cites W1598875012 @default.
• W2765863160 cites W1599557787 @default.
• W2765863160 cites W1654460714 @default.
• W2765863160 cites W1657628981 @default.
• W2765863160 cites W1728066272 @default.
• W2765863160 cites W1734082729 @default.
• W2765863160 cites W1742842239 @default.
• W2765863160 cites W1745634660 @default.
• W2765863160 cites W1764308599 @default.
• W2765863160 cites W1775964807 @default.
• W2765863160 cites W1799692929 @default.
• W2765863160 cites W1813230101 @default.
• W2765863160 cites W1816221338 @default.
• W2765863160 cites W1849928642 @default.
• W2765863160 cites W1850791929 @default.
• W2765863160 cites W1860472154 @default.
• W2765863160 cites W1866713406 @default.
• W2765863160 cites W1903793818 @default.
• W2765863160 cites W1905600998 @default.
• W2765863160 cites W1935060748 @default.
• W2765863160 cites W1963835954 @default.
• W2765863160 cites W1963971594 @default.
• W2765863160 cites W1965745205 @default.
• W2765863160 cites W1966072897 @default.
• W2765863160 cites W1966471287 @default.
• W2765863160 cites W1966694867 @default.
• W2765863160 cites W1968586690 @default.
• W2765863160 cites W1968798075 @default.
• W2765863160 cites W1970094644 @default.
• W2765863160 cites W1970554352 @default.
• W2765863160 cites W1971082641 @default.
• W2765863160 cites W1971269855 @default.
• W2765863160 cites W1972988505 @default.
• W2765863160 cites W1974505849 @default.
• W2765863160 cites W1975167087 @default.
• W2765863160 cites W1976285614 @default.
• W2765863160 cites W1976890482 @default.
• W2765863160 cites W1977352903 @default.
• W2765863160 cites W1977556645 @default.
• W2765863160 cites W1978240280 @default.
• W2765863160 cites W1978631786 @default.
• W2765863160 cites W1978631832 @default.
• W2765863160 cites W1978669254 @default.
• W2765863160 cites W1979127230 @default.
• W2765863160 cites W1979995768 @default.
• W2765863160 cites W1981659420 @default.
• W2765863160 cites W1981921279 @default.
• W2765863160 cites W1981972734 @default.
• W2765863160 cites W1982729063 @default.
• W2765863160 cites W1983737685 @default.
• W2765863160 cites W1983992135 @default.
• W2765863160 cites W1984452029 @default.
• W2765863160 cites W1984797661 @default.
• W2765863160 cites W1985925852 @default.
• W2765863160 cites W1986003236 @default.
• W2765863160 cites W1986956461 @default.
• W2765863160 cites W1987695408 @default.
• W2765863160 cites W1987981231 @default.
• W2765863160 cites W1988230895 @default.
• W2765863160 cites W1990713266 @default.
• W2765863160 cites W1990788579 @default.
• W2765863160 cites W1992390260 @default.

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