FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2087143449> ?p ?o ?g. }

• W2087143449 abstract "Atrial fibrillation remains the most common clinical cardiac arrhythmia, affecting 1-2% of the population [1-6]. It is characterized by uncoordinated depolarization of the atria in an intermittent (paroxysmal or persistent AF) or constant (permanent AF) fashion [7]. AF leads to impaired atrial contraction and is associated with increased morbidity and mortality [8]. Underlying this arrhythmia are specific electrical phenomena controlled by a diverse set of remodeling mechanisms. These electrical phenomena are reentrant waves, rapidly firing ectopic foci, and rotors which in combination can lead to initiation and maintenance of a fibrillating wave pattern [9]. Much of current research has focused on identifying remodeling mechanisms that develop an AF-prone substrate. These mechanisms can be generally grouped into three types: electrical, structural, and autonomic which have been reviewed in greater detail elsewhere [10-12]. Electrical remodeling includes alterations in K+ currents, L-type Ca2+ currents, and gap junction function. Structural remodeling includes atrial fibrosis, size, and ultrastructure. Autonomic remodeling includes hyperinnervation of the atria and surrounding region as well as increased sympathovagal activity. Though research to date has revealed a detailed and complex view of remodeling in AF, the specific myocyte stressors that activate these remodeling mechanisms are less well understood. The factors contributing to initiation of AF include inflammation, cell death, oxidative stress, hypertrophy and fibrosis [10-12]. Human clinical studies as well as mouse models have provided strong evidence of AF secondary to cardiac disease, such as congestive heart failure (CHF) where many of these remodeling mechanisms are activated by the failing heart [13-15]. These mechanisms can also be activated by AF itself, i.e. “AF begets AF,” which leads to progressive worsening of the disease as the atrial substrate becomes more and more AF-prone [16]. In cases of AF occurring independent of other diseases, referred to as lone AF, an understanding of these triggering factors can be especially important. In the recent publication, “Reactive γ-Ketoaldehydes Promote Protein Misfolding and Preamyloid Oligomer Formation in Rapidly-Activated Atrial Cells,” Sidorova et al. identify a new molecular component that may link oxidative stress to the development of an AF-prone substrate [17]. Their study exploits a rapidly-paced atrial cell line model to to mimic early AF stress responses in order to highlight a major role for oxidative stress pathways in atrial myocytes involving γ-ketoaldehydes (γ-KA) in the formation of preamlyoid oligomers (PAO), which are soluble precursors to amyloid deposits." @default.
• W2087143449 created "2016-06-24" @default.
• W2087143449 creator A5069089350 @default.
• W2087143449 creator A5083965570 @default.
• W2087143449 date "2015-03-01" @default.
• W2087143449 modified "2023-09-24" @default.
• W2087143449 title "A new mechanism links preamyloid oligomer formation in the myocyte stress response associated with atrial fibrillation" @default.
• W2087143449 cites W1480924908 @default.
• W2087143449 cites W1489783301 @default.
• W2087143449 cites W1551429746 @default.
• W2087143449 cites W1965323839 @default.
• W2087143449 cites W1970577444 @default.
• W2087143449 cites W1972142091 @default.
• W2087143449 cites W1977156311 @default.
• W2087143449 cites W1984307178 @default.
• W2087143449 cites W2003011197 @default.
• W2087143449 cites W20074729 @default.
• W2087143449 cites W2017179259 @default.
• W2087143449 cites W2023143117 @default.
• W2087143449 cites W2033078172 @default.
• W2087143449 cites W2033557104 @default.
• W2087143449 cites W2037219759 @default.
• W2087143449 cites W2044564411 @default.
• W2087143449 cites W2046511609 @default.
• W2087143449 cites W2050817817 @default.
• W2087143449 cites W2057918262 @default.
• W2087143449 cites W2059833923 @default.
• W2087143449 cites W2061301580 @default.
• W2087143449 cites W2062206620 @default.
• W2087143449 cites W2069866232 @default.
• W2087143449 cites W2074334843 @default.
• W2087143449 cites W2076793021 @default.
• W2087143449 cites W2078504128 @default.
• W2087143449 cites W2080606620 @default.
• W2087143449 cites W2089939521 @default.
• W2087143449 cites W2090138155 @default.
• W2087143449 cites W2098471105 @default.
• W2087143449 cites W2105150315 @default.
• W2087143449 cites W2107020336 @default.
• W2087143449 cites W2116272076 @default.
• W2087143449 cites W2125693777 @default.
• W2087143449 cites W2125729240 @default.
• W2087143449 cites W2126825653 @default.
• W2087143449 cites W2138023380 @default.
• W2087143449 cites W2143016415 @default.
• W2087143449 cites W2148056560 @default.
• W2087143449 cites W2156207648 @default.
• W2087143449 cites W2161841138 @default.
• W2087143449 cites W2167423131 @default.
• W2087143449 cites W2013946241 @default.
• W2087143449 doi "https://doi.org/10.1016/j.yjmcc.2014.12.005" @default.
• W2087143449 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4346451" @default.
• W2087143449 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25541246" @default.
• W2087143449 hasPublicationYear "2015" @default.
• W2087143449 type Work @default.
• W2087143449 sameAs 2087143449 @default.
• W2087143449 citedByCount "0" @default.
• W2087143449 crossrefType "journal-article" @default.
• W2087143449 hasAuthorship W2087143449A5069089350 @default.
• W2087143449 hasAuthorship W2087143449A5083965570 @default.
• W2087143449 hasBestOaLocation W20871434492 @default.
• W2087143449 hasConcept C126322002 @default.
• W2087143449 hasConcept C164705383 @default.
• W2087143449 hasConcept C167414201 @default.
• W2087143449 hasConcept C2778198053 @default.
• W2087143449 hasConcept C2779161974 @default.
• W2087143449 hasConcept C2779537366 @default.
• W2087143449 hasConcept C2780559512 @default.
• W2087143449 hasConcept C2908647359 @default.
• W2087143449 hasConcept C2988455589 @default.
• W2087143449 hasConcept C71924100 @default.
• W2087143449 hasConcept C99454951 @default.
• W2087143449 hasConceptScore W2087143449C126322002 @default.
• W2087143449 hasConceptScore W2087143449C164705383 @default.
• W2087143449 hasConceptScore W2087143449C167414201 @default.
• W2087143449 hasConceptScore W2087143449C2778198053 @default.
• W2087143449 hasConceptScore W2087143449C2779161974 @default.
• W2087143449 hasConceptScore W2087143449C2779537366 @default.
• W2087143449 hasConceptScore W2087143449C2780559512 @default.
• W2087143449 hasConceptScore W2087143449C2908647359 @default.
• W2087143449 hasConceptScore W2087143449C2988455589 @default.
• W2087143449 hasConceptScore W2087143449C71924100 @default.
• W2087143449 hasConceptScore W2087143449C99454951 @default.
• W2087143449 hasFunder F4320306230 @default.
• W2087143449 hasLocation W20871434491 @default.
• W2087143449 hasLocation W20871434492 @default.
• W2087143449 hasLocation W20871434493 @default.
• W2087143449 hasLocation W20871434494 @default.
• W2087143449 hasOpenAccess W2087143449 @default.
• W2087143449 hasPrimaryLocation W20871434491 @default.
• W2087143449 hasRelatedWork W1992753622 @default.
• W2087143449 hasRelatedWork W2049834315 @default.
• W2087143449 hasRelatedWork W2087314277 @default.
• W2087143449 hasRelatedWork W2103543617 @default.
• W2087143449 hasRelatedWork W2273488887 @default.
• W2087143449 hasRelatedWork W2348686897 @default.
• W2087143449 hasRelatedWork W2386750603 @default.
• W2087143449 hasRelatedWork W2391113001 @default.
• W2087143449 hasRelatedWork W2399063111 @default.
• W2087143449 hasRelatedWork W3215129447 @default.

• next