2017
DOI: 10.1016/j.freeradbiomed.2017.08.012
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Advanced glycation end products receptor RAGE controls myocardial dysfunction and oxidative stress in high-fat fed mice by sustaining mitochondrial dynamics and autophagy-lysosome pathway

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Cited by 55 publications
(28 citation statements)
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“…In addition, Hofmann et al have clarified a significant relationship between AGE-modified cardiac tissue collagen and skin AF [ 23 ]. Several pathways by which AGEs or their receptors influence myocardial injury have been reported [ 24 - 26 ]. Furthermore, basic studies have indicated that AGEs influence hemorheology by mechanisms such as platelet aggregation, leukocyte-endothelial interaction and morphological changes in the erythrocyte membrane [ 27 - 29 ].…”
Section: Discussionmentioning
confidence: 99%
“…In addition, Hofmann et al have clarified a significant relationship between AGE-modified cardiac tissue collagen and skin AF [ 23 ]. Several pathways by which AGEs or their receptors influence myocardial injury have been reported [ 24 - 26 ]. Furthermore, basic studies have indicated that AGEs influence hemorheology by mechanisms such as platelet aggregation, leukocyte-endothelial interaction and morphological changes in the erythrocyte membrane [ 27 - 29 ].…”
Section: Discussionmentioning
confidence: 99%
“…In this scenario, it is intriguing that apoptotic- and inflammatory-related intracellular pathways operating in AMD, including TLR/RAGEs, PKC, NF-kB, JAK/STAT, AKT/mTOR, and C3 complement, while impinging on the autophagy machinery and standard proteasomes, engage an alternative cytokine-inducible proteasome isoform, the immunoproteasome [ 38 , 84 , 127 , 164 , 165 , 166 , 167 , 168 , 169 , 170 ]. Contrarily from the standard proteasome, which is ubiquitously expressed, the immunoproteasome operates constitutively in immune tissues and cells, while being induced by oxidative stress and inflammatory cytokines in other kinds of cells, including neurons and glia of the retina and CNS [ 164 ].…”
Section: Cell-clearing Systems In the Rpe As The Keys For Retinal mentioning
confidence: 99%
“…Stressor setting thereby induces synthesis and release of HMGB1 from microglia which triggers the innate immune system (e.g., NLRP3 inflammasome priming) for sensitizing the proinflammatory response of microglia to subsequent immune challenges such as injury and depression, especially during a fight/flight response [13,14]. HMGB1 plays essential roles in the regulation of autophagy in intranuclear, cytosolic, and extracellular compartment, e.g., advanced glycation end product receptor (RAGE) of HMGB1 controls myocardial dysfunction and oxidative stress in high-fat-fed mice by sustaining the mitochondrial dynamics and autophagy-lysosome pathway [15]. However, the detailed mechanisms by which stressors prime microglia-mediated neuroinflammation remain unclear.…”
Section: Introductionmentioning
confidence: 99%