Difference between revisions of "Lu 2022 J Cosmet Dermatol"
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{{Publication | {{Publication | ||
|title=Lu Q, Zou LF, Gao YZ, Ye T, Li MJ, Zhang YK, Liang B, Sun W, Xing DM (2022) Liquiritigenin reverses skin aging by inhibiting UV-induced mitochondrial uncoupling and excessive energy consumption. https://doi.org/10.1111/jocd.15506 | |title=Lu Q, Zou LF, Gao YZ, Ye T, Li MJ, Zhang YK, Liang B, Sun W, Xing DM (2022) Liquiritigenin reverses skin aging by inhibiting UV-induced mitochondrial uncoupling and excessive energy consumption. https://doi.org/10.1111/jocd.15506 | ||
|info=J Cosmet Dermatol | |info=J Cosmet Dermatol 22:1017-30. [https://www.ncbi.nlm.nih.gov/pubmed/36575875 PMID: 36575875 Open Access] | ||
|authors=Lu Qi, Zou Lin-Feng, Gao Yuan-Zhen, Ye Ting, Li Meng-Jiao, Zhang Yu-Kun, Liang Bing, Sun Wenshe, Xing Dong-Ming | |authors=Lu Qi, Zou Lin-Feng, Gao Yuan-Zhen, Ye Ting, Li Meng-Jiao, Zhang Yu-Kun, Liang Bing, Sun Wenshe, Xing Dong-Ming | ||
|year=2022 | |year=2022 | ||
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|abstract=The accumulation of reactive oxygen species (ROS) generated by UV radiation can lead to lipid, protein, nucleic acid, and organelle damage, one of the core mechanisms mediating skin aging. In the photoaging process, how ROS drives the imbalance of the body's complex repair system to induce senescence-like features is not fully understood. | |abstract=The accumulation of reactive oxygen species (ROS) generated by UV radiation can lead to lipid, protein, nucleic acid, and organelle damage, one of the core mechanisms mediating skin aging. In the photoaging process, how ROS drives the imbalance of the body's complex repair system to induce senescence-like features is not fully understood. | ||
We irradiated human epidermal keratinocytes with 12 J/ | We irradiated human epidermal keratinocytes with 12 J/cm<sup>2</sup> of UVA to establish an ''in vitro'' photoaging model. Then we employed whole-transcriptome sequencing and O2K mitochondrial function assay to reveal the photoprotective mechanisms of liquiritigenin (LQ). | ||
We found that skin reduces endogenous ROS by promoting mitochondrial oxidative phosphorylation uncoupling in response to UVA-induced damage. However, this also causes excessive consumption and idling of nutrients, leading to the inhibition of cell proliferation, and ultimately accelerating the skin aging process. Here, we demonstrated that LQ can reduce stress in keratinocytes, increase oxidative phosphorylation and ATP production efficiency, and block the massive loss of skin nutrients and net energy stress. Furthermore, LQ can promote collagen synthesis and keratinocyte proliferation through the PI3K-AKT pathway, thereby reversing photoaging. | We found that skin reduces endogenous ROS by promoting mitochondrial oxidative phosphorylation uncoupling in response to UVA-induced damage. However, this also causes excessive consumption and idling of nutrients, leading to the inhibition of cell proliferation, and ultimately accelerating the skin aging process. Here, we demonstrated that LQ can reduce stress in keratinocytes, increase oxidative phosphorylation and ATP production efficiency, and block the massive loss of skin nutrients and net energy stress. Furthermore, LQ can promote collagen synthesis and keratinocyte proliferation through the PI3K-AKT pathway, thereby reversing photoaging. | ||
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{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration | ||
|diseases=Aging;senescence | |||
|injuries=Oxidative stress;RONS | |||
|organism=Human | |||
|tissues=Endothelial;epithelial;mesothelial cell | |||
|preparations=Intact cells | |||
|couplingstates=LEAK, ROUTINE, ET | |||
|pathways=ROX | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=2023-01 | |additional=2023-01 | ||
}} | }} | ||
Latest revision as of 19:23, 24 February 2023
| Lu Q, Zou LF, Gao YZ, Ye T, Li MJ, Zhang YK, Liang B, Sun W, Xing DM (2022) Liquiritigenin reverses skin aging by inhibiting UV-induced mitochondrial uncoupling and excessive energy consumption. https://doi.org/10.1111/jocd.15506 |
» J Cosmet Dermatol 22:1017-30. PMID: 36575875 Open Access
Lu Qi, Zou Lin-Feng, Gao Yuan-Zhen, Ye Ting, Li Meng-Jiao, Zhang Yu-Kun, Liang Bing, Sun Wenshe, Xing Dong-Ming (2022) J Cosmet Dermatol
Abstract: The accumulation of reactive oxygen species (ROS) generated by UV radiation can lead to lipid, protein, nucleic acid, and organelle damage, one of the core mechanisms mediating skin aging. In the photoaging process, how ROS drives the imbalance of the body's complex repair system to induce senescence-like features is not fully understood.
We irradiated human epidermal keratinocytes with 12 J/cm2 of UVA to establish an in vitro photoaging model. Then we employed whole-transcriptome sequencing and O2K mitochondrial function assay to reveal the photoprotective mechanisms of liquiritigenin (LQ).
We found that skin reduces endogenous ROS by promoting mitochondrial oxidative phosphorylation uncoupling in response to UVA-induced damage. However, this also causes excessive consumption and idling of nutrients, leading to the inhibition of cell proliferation, and ultimately accelerating the skin aging process. Here, we demonstrated that LQ can reduce stress in keratinocytes, increase oxidative phosphorylation and ATP production efficiency, and block the massive loss of skin nutrients and net energy stress. Furthermore, LQ can promote collagen synthesis and keratinocyte proliferation through the PI3K-AKT pathway, thereby reversing photoaging.
This work provides a new skin aging mechanism and solution strategy with high clinical translation value. • Keywords: UVA, Epidermal keratinocytes, Liquiritigenin, Mitochondrial oxidative phosphorylation, Photoaging • Bioblast editor: Plangger M
Labels: MiParea: Respiration
Pathology: Aging;senescence
Stress:Oxidative stress;RONS
Organism: Human
Tissue;cell: Endothelial;epithelial;mesothelial cell
Preparation: Intact cells
Coupling state: LEAK, ROUTINE, ET
Pathway: ROX
HRR: Oxygraph-2k
2023-01
