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Akin, Senay; Kubat, Gokhan B.; Guray, Umit; Akin, Yesim; Demirel, Haydar A.
<?xml version='1.0' encoding='utf-8'?> <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> <dc:creator>Akin, Senay</dc:creator> <dc:creator>Kubat, Gokhan B.</dc:creator> <dc:creator>Guray, Umit</dc:creator> <dc:creator>Akin, Yesim</dc:creator> <dc:creator>Demirel, Haydar A.</dc:creator> <dc:date>2021-01-01</dc:date> <dc:description>Glucocorticoids are among the most prescribed drugs globally due to their potent anti-inflammatory and immunosuppressive properties. Although they have positive effects on the treatment of various disease states; long-term administration is associated with high blood pressure, insulin resistance, and susceptibility to type 2 diabetes. The heart attempts to cope with increased blood pressure and a decrease in glucose utilization by developing pathological cardiac remodeling. However, in this process, cardiac fibrosis formation and deterioration in heart structure and functions occur. Galectin-3, a member of the beta-galactoside binding lectins, is consistently associated with inflammation and fibrosis in the pathogenesis of various disease states including insulin resistance and heart failure. Galectin-3 expression is markedly increased in activated macrophages and a subset of activated fibroblasts and vascular cells. Also, failing and remodeling myocardium show increased Gal-3 expression and elevated Gal-3 levels are related to heart failure severity and prognosis. Furthermore, Gal-3-related pathways are recently suggested as therapeutic targets both pharmacologically and genetically to increase insulin sensitivity in vivo. The objective of this review is to provide a summary of our current understanding of the role of glucocorticoid-associated insulin resistance, which is important for some cardiac events, and the potential role of galectin in this pathophysiological process.</dc:description> <dc:identifier>https://aperta.ulakbim.gov.trrecord/236452</dc:identifier> <dc:identifier>oai:aperta.ulakbim.gov.tr:236452</dc:identifier> <dc:rights>info:eu-repo/semantics/openAccess</dc:rights> <dc:rights>http://www.opendefinition.org/licenses/cc-by</dc:rights> <dc:source>JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY 35(4)</dc:source> <dc:title>Possible value of galectin-3 on follow-up of cardiac remodeling during glucocorticoid treatment</dc:title> <dc:type>info:eu-repo/semantics/article</dc:type> <dc:type>publication-article</dc:type> </oai_dc:dc>
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