2021
DOI: 10.1016/j.fct.2021.112351
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Palmitoyl-CoA effect on cytochrome c release, a key process of apoptosis, from liver mitochondria of rat with sucrose diet-induced obesity

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Cited by 11 publications
(8 citation statements)
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“…In fact, Bax is a pro‐apoptotic protein which can eliminate the membrane potential of mitochondria and promote the release of Cyt.c by affecting PTP. As for Bcl‐2, it is an anti‐apoptotic protein that can preserve the membrane potential and block the release of Cyt.c 23,24 . In this study, PRP significantly decreased the protein levels of Bax and Cyt.c while notably increased the protein levels of Bcl‐2 in UVB‐irradiated HaCaT cells.…”
Section: Discussionsupporting
confidence: 49%
See 1 more Smart Citation
“…In fact, Bax is a pro‐apoptotic protein which can eliminate the membrane potential of mitochondria and promote the release of Cyt.c by affecting PTP. As for Bcl‐2, it is an anti‐apoptotic protein that can preserve the membrane potential and block the release of Cyt.c 23,24 . In this study, PRP significantly decreased the protein levels of Bax and Cyt.c while notably increased the protein levels of Bcl‐2 in UVB‐irradiated HaCaT cells.…”
Section: Discussionsupporting
confidence: 49%
“…As for Bcl-2, it is an anti-apoptotic protein that can preserve the membrane potential and block the release of Cyt.c. 23,24 In this study, PRP significantly decreased the protein levels of Bax and Cyt.c while notably thereby modifying or regulating the folding of proteins. 31 CHOP is a specific mediator for the ER stress-induced apoptosis pathway.…”
Section: Discussionmentioning
confidence: 53%
“…Thus, we speculate that compound 32, by down-regulating the expression of mitochondrial cytochrome C protein, prevents normal electron transport of the respiratory chain and the accumulation of ROS, which eventually causes iron death [38]. On the other hand, cytochrome C is a key substance for mitochondria to initiate the apoptotic program [39], and apoptosis plays a vital role in maintaining the normal physiological homeostasis of the organism and removing senescent cells from the organism [40]. Reduced expression of mitochondrial cytochrome C protein inhibited the apoptotic effect and affected the normal growth and development of Plutella xylostella.…”
Section: Kegg Classification Analysismentioning
confidence: 99%
“…Dysregulation of uptake, utilization, and/or storage of triglycerides and FFA [ 4 , 5 ] leads to accumulation of bioactive molecules such as acyl-CoA and ceramides [ 6 , 7 ] triggering pathways including mitogen-activated protein kinase (MAPK), extracellular-signal-regulated kinase (ERK), sterol regulatory element binding protein-1c (SREBP-1c), and uncoupling protein 2 (UCP2) or promoting release of intracellular Ca storages [ 8–11 ]. Apart from diabetes research, lipotoxicity plays a role in the pathogenesis of non-alcoholic fatty liver disease [ 12 ], cardiovascular disease [ 13 ], and apoptosis promoted by cytochrome C release [ 14 ]. Therefore, establishment of standardized protocols for in vitro models with defined FFA as lipid stressors is required for the investigation of underlying mechanisms.…”
Section: Introductionmentioning
confidence: 99%