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A Novel Mechanism of Salvianolic Acid B in Postmyocardial Infarction Cardiac Protection: PHB1-Driven Raf-ERK Pathway
Ce Cao1, Bo Ma2, Jian Zhang3
1National Clinical Research Center for Chinese Medicine Cardiology Beijing Key Laboratory of Chinese Materia Pharmacology Xiyuan Hospital of China Academy of Chinese Medical Sciences Beijing China.
Insights
Salvianolic acid B (SalB) promotes heart cell regeneration after heart attack by activating the Raf-ERK pathway through Prohibitin 1 (PHB1). This novel mechanism aids in restoring cardiac function and treating heart failure.
Area of Science:
- Cardiology
- Molecular Biology
- Pharmacology
Background:
- Heart failure (HF) post-myocardial infarction is a major global health concern.
- Salvianolic acid B (SalB), from Salvia miltiorrhiza, shows potential in reversing cardiac damage.
- Novel therapeutic strategies are needed to improve cardiac function after infarction.
Purpose of the Study:
- To elucidate the mechanism of SalB in treating post-myocardial infarction heart failure.
- To identify the protein target of SalB responsible for its cardioprotective effects.
- To investigate SalB's role in promoting cardiomyocyte cell cycle re-entry.
Main Methods:
- Chemical biology techniques for target identification.
- Overexpression and knockdown experiments for Prohibitin 1 (PHB1).
- Molecular dynamics simulations to analyze protein-ligand interactions and pathway activation.
Main Results:
- SalB targets Prohibitin 1 (PHB1) to promote cardiomyocyte mitosis.
- SalB upregulates the phosphorylation of the Raf-ERK pathway via PHB1.
- SalB binds to PHB1/2 heterodimer, inducing conformational changes that enhance Raf-ERK activation through Akt-mediated phosphorylation.
Conclusions:
- SalB promotes cardiomyocyte cell cycle re-entry, offering a new therapeutic approach for heart failure.
- The PHB1-Raf-ERK pathway is a key mediator of SalB's cardioprotective effects.
- This study reveals a novel molecular mechanism for SalB in preserving and restoring cardiac function.
Abstract:
Heart failure (HF) following myocardial infarction remains a leading cause of global morbidity and mortality, necessitating novel therapeutic strategies. Salvianolic acid B (SalB), one of the major active components of Salvia miltiorrhiza Bunge, has been shown to effectively reverse ischemia-induced myocardial infarction and improve cardiac function. Here, we report a novel mechanism by which SalB treats postmyocardial infarction heart failure by promoting cardiomyocyte re-entry into the cell cycle. A novel protein target of SalB, Prohibitin 1 (PHB1), was identified using chemical biology techniques. Experiments involving overexpression and knockdown of PHB1 have demonstrated that SalB promotes cardiomyocyte mitosis by acting on PHB1, which in turn upregulates the phosphorylation level of the Raf-ERK pathway. Molecular dynamics simulations provide a comprehensive explanation for the mechanism by which SalB enhances Raf phosphorylation. The findings reveal that SalB binds to the C-terminal of PHB1/2 heterodimer, inducing a conformational change that enhances Raf-ERK pathway activation via Akt-mediated phosphorylation, thereby promoting cardiomyocyte mitosis. The findings of this study propose a promising new molecular mechanism through which SalB can contribute to the preservation and restoration of cardiac function.
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