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• W2897586248 abstract "Type 2 diabetes (T2D) is a major risk factor for heart failure. Diabetic cardiomyopathy (DC) is characterized by diastolic dysfunction and left ventricular hypertrophy. Epidemiological data suggest that hyperglycaemia contributes to the development of DC. Several cellular pathways have been implicated in the deleterious effects of high glucose concentrations in the heart: oxidative stress, accumulation of advanced glycation end products (AGE), and chronic hexosamine biosynthetic pathway (HBP) activation. In the present review, we focus on the effect of chronic activation of the HBP on diabetic heart function. The HBP supplies N-acetylglucosamine moiety (O-GlcNAc) that is O-linked by O-GlcNAc transferase (OGT) to proteins on serine or threonine residues. This post-translational protein modification modulates the activity of the targeted proteins. In the heart, acute activation of the HBP in response to ischaemia-reperfusion injury appears to be protective. Conversely, chronic activation of the HBP in the diabetic heart affects Ca2+ handling, contractile properties, and mitochondrial function and promotes stress signaling, such as left ventricular hypertrophy and endoplasmic reticulum stress. Many studies have shown that O-GlcNAc impairs the function of key protein targets involved in these pathways, such as phospholamban, calmodulin kinase II, troponin I, and FOXO1. The data show that excessive O-GlcNAcylation is a major trigger of the glucotoxic events that affect heart function under chronic hyperglycaemia. Supporting this finding, pharmacological or genetic inhibition of the HBP in the diabetic heart improves heart function. In addition, the SGLT2 inhibitor dapagliflozin, a glucose lowering agent, has recently been shown to lower cardiac HBP in a lipodystophic T2D mice model and to concomitantly improve the diastolic dysfunction of these mice. Therefore, targeting cardiac-excessive O-GlcNAcylation or specific target proteins represents a potential therapeutic option to treat glucotoxicity in the diabetic heart." @default.
• W2897586248 created "2018-10-26" @default.
• W2897586248 creator A5009182471 @default.
• W2897586248 creator A5039962721 @default.
• W2897586248 creator A5053756068 @default.
• W2897586248 creator A5081536133 @default.
• W2897586248 date "2018-10-29" @default.
• W2897586248 modified "2023-10-18" @default.
• W2897586248 title "Chronic O-GlcNAcylation and Diabetic Cardiomyopathy: The Bitterness of Glucose" @default.
• W2897586248 cites W1590732591 @default.
• W2897586248 cites W1715909735 @default.
• W2897586248 cites W1878567746 @default.
• W2897586248 cites W1966498072 @default.
• W2897586248 cites W1968223043 @default.
• W2897586248 cites W1969698093 @default.
• W2897586248 cites W1971412377 @default.
• W2897586248 cites W1972142752 @default.
• W2897586248 cites W1975959667 @default.
• W2897586248 cites W1976696759 @default.
• W2897586248 cites W1982283232 @default.
• W2897586248 cites W1982380248 @default.
• W2897586248 cites W1985039567 @default.
• W2897586248 cites W1986276307 @default.
• W2897586248 cites W1990634680 @default.
• W2897586248 cites W1992897888 @default.
• W2897586248 cites W1993790829 @default.
• W2897586248 cites W1996451200 @default.
• W2897586248 cites W1996539872 @default.
• W2897586248 cites W2000325349 @default.
• W2897586248 cites W2000521653 @default.
• W2897586248 cites W2000773294 @default.
• W2897586248 cites W2013684433 @default.
• W2897586248 cites W2018559323 @default.
• W2897586248 cites W2022143285 @default.
• W2897586248 cites W2025446061 @default.
• W2897586248 cites W2026199993 @default.
• W2897586248 cites W2028240468 @default.
• W2897586248 cites W2028533363 @default.
• W2897586248 cites W2032916059 @default.
• W2897586248 cites W2037526260 @default.
• W2897586248 cites W2042206853 @default.
• W2897586248 cites W2044370075 @default.
• W2897586248 cites W2044741742 @default.
• W2897586248 cites W2054203136 @default.
• W2897586248 cites W2058370904 @default.
• W2897586248 cites W2058536977 @default.
• W2897586248 cites W2062383366 @default.
• W2897586248 cites W2067056774 @default.
• W2897586248 cites W2072203364 @default.
• W2897586248 cites W2073900053 @default.
• W2897586248 cites W2074332237 @default.
• W2897586248 cites W2075358633 @default.
• W2897586248 cites W2077805551 @default.
• W2897586248 cites W2078266069 @default.
• W2897586248 cites W2078330387 @default.
• W2897586248 cites W2078633259 @default.
• W2897586248 cites W2081098379 @default.
• W2897586248 cites W2090556647 @default.
• W2897586248 cites W2094005996 @default.
• W2897586248 cites W2105731956 @default.
• W2897586248 cites W2106842409 @default.
• W2897586248 cites W2107746022 @default.
• W2897586248 cites W2109282106 @default.
• W2897586248 cites W2109485511 @default.
• W2897586248 cites W2113181569 @default.
• W2897586248 cites W2115088504 @default.
• W2897586248 cites W2115419925 @default.
• W2897586248 cites W2116532275 @default.
• W2897586248 cites W2116979101 @default.
• W2897586248 cites W2120416709 @default.
• W2897586248 cites W2120647467 @default.
• W2897586248 cites W2127321192 @default.
• W2897586248 cites W2128536736 @default.
• W2897586248 cites W2130135884 @default.
• W2897586248 cites W2134013131 @default.
• W2897586248 cites W2137712469 @default.
• W2897586248 cites W2140069893 @default.
• W2897586248 cites W2140409722 @default.
• W2897586248 cites W2144766505 @default.
• W2897586248 cites W2147909043 @default.
• W2897586248 cites W2151864871 @default.
• W2897586248 cites W2153092921 @default.
• W2897586248 cites W2156420062 @default.
• W2897586248 cites W2158147445 @default.
• W2897586248 cites W2158333126 @default.
• W2897586248 cites W2162349906 @default.
• W2897586248 cites W2165832533 @default.
• W2897586248 cites W2167251566 @default.
• W2897586248 cites W2187158970 @default.
• W2897586248 cites W2218334377 @default.
• W2897586248 cites W2294945370 @default.
• W2897586248 cites W2397197700 @default.
• W2897586248 cites W2399659685 @default.
• W2897586248 cites W2471605942 @default.
• W2897586248 cites W2513893629 @default.
• W2897586248 cites W2518341489 @default.
• W2897586248 cites W2548392462 @default.
• W2897586248 cites W2550251732 @default.
• W2897586248 cites W2566332558 @default.
• W2897586248 cites W2568435816 @default.

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