FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2013048175> ?p ?o ?g. }

• W2013048175 endingPage "27" @default.
• W2013048175 startingPage "1" @default.
• W2013048175 abstract "It is well established that regular physiological stimulation by glucose plays a crucial role in the maintenance of the β-cell differentiated phenotype. In contrast, prolonged or repeated exposure to elevated glucose concentrations both in vitro and in vivo exerts deleterious or toxic effects on the β-cell phenotype, a concept termed as glucotoxicity. Evidence indicates that the latter may greatly contribute to the pathogenesis of type 2 diabetes. Through the activation of several mechanisms and signaling pathways, high glucose levels exert deleterious effects on β-cell function and survival and thereby, lead to the worsening of the disease over time. While the role of high glucose-induced β-cell overstimulation, oxidative stress, excessive Unfolded Protein Response (UPR) activation, and loss of differentiation in the alteration of the β-cell phenotype is well ascertained, at least in vitro and in animal models of type 2 diabetes, the role of other mechanisms such as inflammation, O-GlcNacylation, PKC activation, and amyloidogenesis requires further confirmation. On the other hand, protein glycation is an emerging mechanism that may play an important role in the glucotoxic deterioration of the β-cell phenotype. Finally, our recent evidence suggests that hypoxia may also be a new mechanism of β-cell glucotoxicity. Deciphering these molecular mechanisms of β-cell glucotoxicity is a mandatory first step toward the development of therapeutic strategies to protect β-cells and improve the functional β-cell mass in type 2 diabetes." @default.
• W2013048175 created "2016-06-24" @default.
• W2013048175 creator A5013533504 @default.
• W2013048175 creator A5053931632 @default.
• W2013048175 creator A5086237869 @default.
• W2013048175 date "2012-11-01" @default.
• W2013048175 modified "2023-10-07" @default.
• W2013048175 title "The molecular mechanisms of pancreatic β-cell glucotoxicity: Recent findings and future research directions" @default.
• W2013048175 cites W11872906 @default.
• W2013048175 cites W121348928 @default.
• W2013048175 cites W1505761263 @default.
• W2013048175 cites W1516670301 @default.
• W2013048175 cites W1543532453 @default.
• W2013048175 cites W1544514004 @default.
• W2013048175 cites W1545562191 @default.
• W2013048175 cites W1547647973 @default.
• W2013048175 cites W1559266759 @default.
• W2013048175 cites W1561949950 @default.
• W2013048175 cites W1584646599 @default.
• W2013048175 cites W1588092320 @default.
• W2013048175 cites W1594523559 @default.
• W2013048175 cites W1602411554 @default.
• W2013048175 cites W1605496649 @default.
• W2013048175 cites W1650754258 @default.
• W2013048175 cites W1674418446 @default.
• W2013048175 cites W173210163 @default.
• W2013048175 cites W1847251007 @default.
• W2013048175 cites W1851126014 @default.
• W2013048175 cites W1864559392 @default.
• W2013048175 cites W1865758164 @default.
• W2013048175 cites W1892916724 @default.
• W2013048175 cites W1922087192 @default.
• W2013048175 cites W1927620573 @default.
• W2013048175 cites W1932654578 @default.
• W2013048175 cites W1963741325 @default.
• W2013048175 cites W1964459403 @default.
• W2013048175 cites W1964627768 @default.
• W2013048175 cites W1965456684 @default.
• W2013048175 cites W1965709403 @default.
• W2013048175 cites W1965729726 @default.
• W2013048175 cites W1966156012 @default.
• W2013048175 cites W1966351825 @default.
• W2013048175 cites W1966419887 @default.
• W2013048175 cites W1966598176 @default.
• W2013048175 cites W1967005515 @default.
• W2013048175 cites W1967287226 @default.
• W2013048175 cites W1967766455 @default.
• W2013048175 cites W1967964480 @default.
• W2013048175 cites W1968237817 @default.
• W2013048175 cites W1968368398 @default.
• W2013048175 cites W1969047353 @default.
• W2013048175 cites W1970290322 @default.
• W2013048175 cites W1971069803 @default.
• W2013048175 cites W1971654760 @default.
• W2013048175 cites W1971925153 @default.
• W2013048175 cites W1972156839 @default.
• W2013048175 cites W1973794425 @default.
• W2013048175 cites W1974113995 @default.
• W2013048175 cites W1974558745 @default.
• W2013048175 cites W1975347125 @default.
• W2013048175 cites W1975877581 @default.
• W2013048175 cites W1976339688 @default.
• W2013048175 cites W1976907809 @default.
• W2013048175 cites W1977703892 @default.
• W2013048175 cites W1978463531 @default.
• W2013048175 cites W1978613422 @default.
• W2013048175 cites W1978982940 @default.
• W2013048175 cites W1979182598 @default.
• W2013048175 cites W1979946833 @default.
• W2013048175 cites W1980026278 @default.
• W2013048175 cites W1981618191 @default.
• W2013048175 cites W1982204392 @default.
• W2013048175 cites W1982293047 @default.
• W2013048175 cites W1983099475 @default.
• W2013048175 cites W1983655800 @default.
• W2013048175 cites W1984262473 @default.
• W2013048175 cites W1984597516 @default.
• W2013048175 cites W1987735363 @default.
• W2013048175 cites W1988077890 @default.
• W2013048175 cites W1988453786 @default.
• W2013048175 cites W1988609240 @default.
• W2013048175 cites W1989245431 @default.
• W2013048175 cites W1989540914 @default.
• W2013048175 cites W1989762800 @default.
• W2013048175 cites W1990093198 @default.
• W2013048175 cites W1990805809 @default.
• W2013048175 cites W1991007222 @default.
• W2013048175 cites W1991049796 @default.
• W2013048175 cites W1991113982 @default.
• W2013048175 cites W1992335598 @default.
• W2013048175 cites W1992622882 @default.
• W2013048175 cites W1992716613 @default.
• W2013048175 cites W1992744425 @default.
• W2013048175 cites W1992788957 @default.
• W2013048175 cites W1993378987 @default.
• W2013048175 cites W1994026558 @default.
• W2013048175 cites W1999806215 @default.
• W2013048175 cites W2000047428 @default.

• next