ReferenceID 6143
Rhein ameliorates transverse aortic constriction-induced cardiac hypertrophy via regulating STAT3 and p38 MAPK signaling pathways
Front Pharmacol
The progression from compensatory hypertrophy to heart failure is difficult to reverse, in part due to extracellular matrix fibrosis and continuous activation of abnormal signaling pathways. Although the anthraquinone rh
Relationship Network
Interactive first-hop connections across herbs, ingredients, formulas, targets, diseases, symptoms, syndromes, evidence, and monographs.
Click a node to open it in a new tab
Ingredient: 1Reference: 1Links: 1
Arranging relationship network...
Record Fields
Scalar fields from the final reference record.
- Reference Id
- 6143
- Evidence Id
- 22733
- Core Evidence Id
- 22733
- Source Reference Id
- 5547
- Herb2 Reference Id
- HBREF006344
- Subject Paper Key
- HBIN042199_36091816
- Pubmed Id
- 36091816
- Doi
- 10.3389/fphar.2022.940574
- Paper Title
- Rhein ameliorates transverse aortic constriction-induced cardiac hypertrophy via regulating STAT3 and p38 MAPK signaling pathways
- Paper Abstract
- The progression from compensatory hypertrophy to heart failure is difficult to reverse, in part due to extracellular matrix fibrosis and continuous activation of abnormal signaling pathways. Although the anthraquinone rhein has been examined for its many biological properties, it is not clear whether it has therapeutic value in the treatment of cardiac hypertrophy and heart failure. In this study, we report for the first time that rhein can ameliorate transverse aortic constriction (TAC)-induced cardiac hypertrophy and other cardiac damage in vivo and in vitro . In addition, rhein can reduce cardiac hypertrophy by attenuating atrial natriuretic peptide, brain natriuretic peptide, and β-MHC expression; cardiac fibrosis; and ERK phosphorylation and transport into the nucleus. Furthermore, the inhibitory effect of rhein on myocardial hypertrophy was similar to that of specific inhibitors of STAT3 and ERK signaling. In addition, rhein at therapeutic doses had no significant adverse effects or toxicity on liver and kidney function. We conclude that rhein reduces TAC-induced cardiac hypertrophy via targeted inhibition of the molecular function of ERK and downregulates STAT3 and p38 MAPK signaling. Therefore, rhein might be a novel and effective agent for treating cardiac hypertrophy and other cardiovascular diseases.
- Journal
- Front Pharmacol
- Publish Year
- 2022
- Experiment Subject
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Transverse Aortic Constriction; Myocardial Hypertrophy; Cardiovascular Diseases; Cardiac Hypertrophy; Compensatory Hypertrophy; Heart Failure; Extracellular Matrix Fibrosis; Cardiac Damage; Cardiac Fibrosis
- Paper Title Cn
- Paper Title En
- Rhein ameliorates transverse aortic constriction-induced cardiac hypertrophy via regulating STAT3 and p38 MAPK signaling pathways
- Bilingual Status
- semi_complete