ReferenceID 5624
Lutein attenuates angiotensin II- induced cardiac remodeling by inhibiting AP-1/IL-11 signaling
Redox Biol
RATIONALE: Oxidative stress plays a critical role in the development of cardiac remodeling and heart failure. Lutein, the predominant nonvitamin A carotenoid, has been shown to have profound effects on oxidative stress.
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Record Fields
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- Reference Id
- 5624
- Evidence Id
- 22214
- Core Evidence Id
- 22214
- Source Reference Id
- 4474
- Herb2 Reference Id
- HBREF005271
- Subject Paper Key
- HBIN033793_34077894
- Pubmed Id
- 34077894
- Doi
- 10.1016/j.redox.2021.102020
- Paper Title
- Lutein attenuates angiotensin II- induced cardiac remodeling by inhibiting AP-1/IL-11 signaling
- Paper Abstract
- RATIONALE: Oxidative stress plays a critical role in the development of cardiac remodeling and heart failure. Lutein, the predominant nonvitamin A carotenoid, has been shown to have profound effects on oxidative stress. However, the effect of lutein on angiotensin II (Ang II)-induced cardiac remodeling and heart failure remains unknown. OBJECTIVE: The aim of this study was to determine whether lutein is involved in cardiac remodeling and to elucidate the underlying molecular mechanisms. METHODS AND RESULTS: In vitro experiments with isolated neonatal rat cardiomyocytes (NRCMs) and cardiac fibroblasts (CFs) revealed that lutein significantly attenuated Ang II-induced collagen expression in CFs, and cardiomyocyte hypertrophy. The Ang II-induced increases in superoxide generation, inflammation and apoptosis in cultured CFs were strikingly prevented by lutein. In vivo, fibrosis, hypertrophic cardiomyocyte and superoxide generation were analyzed, and lutein was demonstrated to confer resistance to Ang II-induced cardiac remodeling in mice. Mechanistically, RNA sequencing revealed that interleukin-11 (IL-11) expression was significantly upregulated in mouse hearts in response to Ang II infusion and was significantly suppressed in the hearts of lutein-treated mice. Furthermore, IL-11 overexpression blocked the effects of lutein on fibrosis and oxidative stress in CFs and impaired the protective effect of lutein on cardiac remodeling. Notably, we discovered that lutein could reduce Ang II-induced IL-11 expression, at least partly through the regulation of activator protein (AP)-1 expression and activity. CONCLUSIONS: Lutein has potential as a treatment for cardiac remodeling and heart failure via the suppression of IL-11 expression.
- Journal
- Redox Biol
- Publish Year
- 2021
- Experiment Subject
- mouse; rat; cultured cfs
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Fibrosis; Cardiomyocyte Hypertrophy; Heart Failure; Cardiac Remodeling
- Paper Title Cn
- Paper Title En
- Lutein attenuates angiotensin II- induced cardiac remodeling by inhibiting AP-1/IL-11 signaling
- Bilingual Status
- semi_complete