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Canthaxanthin Mitigates Cardiovascular Senescence in Vitro and in Vivo
Zhefeng Wang1,2,3,4, Wenxing Liu2, Min Zhang2,3
1Clinical Center for Biotherapy, Central Laboratory, Zhongshan Hospital (Xiamen), Fudan University, 361015 Xiamen, Fujian, China.
Insights
Canthaxanthin effectively combats cardiac aging and fibrosis. This study shows its potential to alleviate cardiomyocyte senescence, offering a new therapeutic avenue for age-related cardiovascular diseases.
Area of Science:
- Gerontology
- Cardiovascular Medicine
- Pharmacology
Background:
- Cardiovascular disease (CVD) risk significantly increases with age, with over 90% of cases occurring in older populations.
- Aging is a primary risk factor for cardiovascular disease, necessitating strategies to slow cardiac aging.
Purpose of the Study:
- To investigate the potential of canthaxanthin in preventing and treating cardiovascular aging.
- To evaluate the effects of canthaxanthin on cardiomyocyte senescence and cardiac fibrosis in aging models.
Main Methods:
- Established an in vitro model of cardiomyocyte senescence induced by D-galactose.
- Conducted in vivo experiments using an aged mice model to assess canthaxanthin's effects.
- Investigated the underlying mechanisms, including the regulation of autophagy.
Main Results:
- Canthaxanthin demonstrated a significant mitigation of cardiomyocyte senescence in vitro.
- Mechanistic studies indicated that canthaxanthin alleviates senescence by regulating autophagy.
- In vivo studies confirmed that canthaxanthin reduces cardiac aging and fibrosis in aged mice.
Conclusions:
- Canthaxanthin effectively alleviates premature cardiac aging and fibrosis.
- Canthaxanthin shows promise as a therapeutic molecule for treating cardiac aging and related fibrotic conditions.
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.
