2023
DOI: 10.1016/j.freeradbiomed.2023.03.264
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Transient inhibition of mitochondrial function by chrysin and apigenin prolong longevity via mitohormesis in C. elegans

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Cited by 7 publications
(3 citation statements)
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“…In a separate transgenic Drosophila model of Alzheimer’s disease (AD) expressing Amyloid Beta-42 in neurons and producing AD-like amyloid beta aggregates, a daily diet containing apigenin for 30 days was shown to delay the loss of climbing typically seen in this model ( 70 ). Apigenin similarly increases survival in a fly model of PD ( 54 ) and, in Caenorhabditis elegans , dietary supplementation with apigenin or apigenin glycosides increases lifespan ( 93 , 94 ).…”
Section: Apigenin and Agingmentioning
confidence: 99%
See 1 more Smart Citation
“…In a separate transgenic Drosophila model of Alzheimer’s disease (AD) expressing Amyloid Beta-42 in neurons and producing AD-like amyloid beta aggregates, a daily diet containing apigenin for 30 days was shown to delay the loss of climbing typically seen in this model ( 70 ). Apigenin similarly increases survival in a fly model of PD ( 54 ) and, in Caenorhabditis elegans , dietary supplementation with apigenin or apigenin glycosides increases lifespan ( 93 , 94 ).…”
Section: Apigenin and Agingmentioning
confidence: 99%
“…This, in turn, triggered a mitohormetic response which led to an overall increased capacity to deal with oxidative stress. Life extension also depended on the genes aak-2 , daf-16 , and skn-1 ( 94 ). Such findings are interesting given that, in a mouse model of myocardial injury, the protective effects of apigenin were dependent on the mitochondrial unfolded protein response ( 99 ).…”
Section: Apigenin and Agingmentioning
confidence: 99%
“…UPRmt genes are upregulated in Alzheimer’s disease (AD), PD, and other neurodegenerative diseases, suggesting a protective role against protein aggregation interfering with mitochondrial function [ 104 , 105 ]. Studies have shown that compounds like chrysanthemum and apigenin can inhibit mitochondrial respiration temporarily, induce early ROS production, and activate the AMPK/NRF-2/FOXO pathway, thereby promoting mitosis, enhancing oxidative stress capacity and cellular metabolic adaptation, and extending the lifespan of C. elegans [ 106 ]. These compounds delay aging and improve age-related diseases by targeting mitochondrial function, suggesting potential therapeutic strategies for mitigating neurodegeneration and aging-related decline.…”
Section: Mitochondrial Stress and Diseasementioning
confidence: 99%