Canthaxanthin Mitigates Cardiovascular Senescence in Vitro and in Vivo
Background: The number of older people in the world is increasing year by year; studies have shown that more than 90% of cardiovascular disease occurs in the older people population, indicating that aging is one of the major risks involved in the development of cardiovascular disease. Therefore, ret...
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IMR Press
2024-02-01
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Series: | Frontiers in Bioscience-Landmark |
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Online Access: | https://www.imrpress.com/journal/FBL/29/2/10.31083/j.fbl2902070 |
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author | Zhefeng Wang Wenxing Liu Min Zhang Jianlong Yan Jia Fei Keda Zhang Shaohong Dong |
author_facet | Zhefeng Wang Wenxing Liu Min Zhang Jianlong Yan Jia Fei Keda Zhang Shaohong Dong |
author_sort | Zhefeng Wang |
collection | DOAJ |
description | Background: The number of older people in the world is increasing year by year; studies have shown that more than 90% of cardiovascular disease occurs in the older people population, indicating that aging is one of the major risks involved in the development of cardiovascular disease. Therefore, retarding the development of cardiac aging is an important strategy to prevent aging-related cardiovascular diseases. Methods: In the current study, we examined the anti-cardiovascular aging potential of canthaxanthin in vitro and in vivo experiments. For this, a model of cardiomyocyte senescence induced by D-galactose was established, which was used to investigate the canthaxanthin’s effect on cardiac premature aging. Results: We found that canthaxanthin obviously mitigated the cardiomyocyte senescence in vitro. Further mechanistic studies revealed that canthaxanthin seems to alleviate cardiomyocyte senescence by regulating the autophagy process. Furthermore, the effects of canthaxanthin on cardiovascular senescence were further evaluated. We also observed that canthaxanthin mitigated cardiac aging and fibrosis in the aged mice model. Conclusions: To sum up, the current work showed that canthaxanthin could obviously alleviate cardiac premature aging, indicating that canthaxanthin could be used as a biologically active molecule for the treatment of cardiac aging and fibrosis. |
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format | Article |
id | doaj.art-b1c97c2229324fe7934e5dd960d9840a |
institution | Directory Open Access Journal |
issn | 2768-6701 |
language | English |
last_indexed | 2024-03-07T19:22:09Z |
publishDate | 2024-02-01 |
publisher | IMR Press |
record_format | Article |
series | Frontiers in Bioscience-Landmark |
spelling | doaj.art-b1c97c2229324fe7934e5dd960d9840a2024-02-29T09:53:15ZengIMR PressFrontiers in Bioscience-Landmark2768-67012024-02-012927010.31083/j.fbl2902070S2768-6701(23)01073-0Canthaxanthin Mitigates Cardiovascular Senescence in Vitro and in VivoZhefeng Wang0Wenxing Liu1Min Zhang2Jianlong Yan3Jia Fei4Keda Zhang5Shaohong Dong6Clinical Center for Biotherapy, Central Laboratory, Zhongshan Hospital (Xiamen), Fudan University, 361015 Xiamen, Fujian, ChinaDepartment of Cardiology, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), 518020 Shenzhen, Guangdong, ChinaDepartment of Cardiology, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), 518020 Shenzhen, Guangdong, ChinaDepartment of Cardiology, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), 518020 Shenzhen, Guangdong, ChinaIntegrated Chinese and Western Medicine Postdoctoral Research Station, Jinan University, 510632 Guangzhou, Guangdong, ChinaCollege of Pharmacy, Shenzhen Technology University, 518118 Shenzhen, Guangdong, ChinaDepartment of Cardiology, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), 518020 Shenzhen, Guangdong, ChinaBackground: The number of older people in the world is increasing year by year; studies have shown that more than 90% of cardiovascular disease occurs in the older people population, indicating that aging is one of the major risks involved in the development of cardiovascular disease. Therefore, retarding the development of cardiac aging is an important strategy to prevent aging-related cardiovascular diseases. Methods: In the current study, we examined the anti-cardiovascular aging potential of canthaxanthin in vitro and in vivo experiments. For this, a model of cardiomyocyte senescence induced by D-galactose was established, which was used to investigate the canthaxanthin’s effect on cardiac premature aging. Results: We found that canthaxanthin obviously mitigated the cardiomyocyte senescence in vitro. Further mechanistic studies revealed that canthaxanthin seems to alleviate cardiomyocyte senescence by regulating the autophagy process. Furthermore, the effects of canthaxanthin on cardiovascular senescence were further evaluated. We also observed that canthaxanthin mitigated cardiac aging and fibrosis in the aged mice model. Conclusions: To sum up, the current work showed that canthaxanthin could obviously alleviate cardiac premature aging, indicating that canthaxanthin could be used as a biologically active molecule for the treatment of cardiac aging and fibrosis.https://www.imrpress.com/journal/FBL/29/2/10.31083/j.fbl2902070cardiovascular agingcanthaxanthinfibrosisp16autophagy |
spellingShingle | Zhefeng Wang Wenxing Liu Min Zhang Jianlong Yan Jia Fei Keda Zhang Shaohong Dong Canthaxanthin Mitigates Cardiovascular Senescence in Vitro and in Vivo Frontiers in Bioscience-Landmark cardiovascular aging canthaxanthin fibrosis p16 autophagy |
title | Canthaxanthin Mitigates Cardiovascular Senescence in Vitro and in Vivo |
title_full | Canthaxanthin Mitigates Cardiovascular Senescence in Vitro and in Vivo |
title_fullStr | Canthaxanthin Mitigates Cardiovascular Senescence in Vitro and in Vivo |
title_full_unstemmed | Canthaxanthin Mitigates Cardiovascular Senescence in Vitro and in Vivo |
title_short | Canthaxanthin Mitigates Cardiovascular Senescence in Vitro and in Vivo |
title_sort | canthaxanthin mitigates cardiovascular senescence in vitro and in vivo |
topic | cardiovascular aging canthaxanthin fibrosis p16 autophagy |
url | https://www.imrpress.com/journal/FBL/29/2/10.31083/j.fbl2902070 |
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