Salvianolic acid A alleviates heart failure with preserved ejection fraction via regulating TLR/Myd88/TRAF/NF-κB and p38MAPK/CREB signaling pathways

Dawuti, Awaguli; Sun, Shuchan; Wang, Ranran; Gong, Difei; Liu, Ruiqi; Kong, Dewen; Yuan, Tianyi; Zhou, Jian; Lu, Yang; Wang, Shoubao; Du, Guanhua; Fang, Lianhua

doi:10.1016/j.biopha.2023.115837

Cited by 11 publications

(2 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Sal A has shown significant effects in the treatment of cardiovascular diseases; however, current research is insufficient to draw a clear conclusion regarding its specific role and effectiveness in protecting against cardiac fibrosis. Clarifying the potential of Sal A in preventing and treating cardiac fibrosis is crucial for reducing fibrosis and regulating cardiac remodeling (26–29).…”

Section: Discussionmentioning

confidence: 99%

Salvianolic Acid a Attenuates Angiotensin Ii-Induced Cardiac Fibrosis Through Regulating the Txnip Signaling Pathway

Ye,

Wang,

et al. 2024

Shock

View full text Add to dashboard Cite

Cardiac fibrosis, characterized by excessive collagen accumulation in heart tissues, poses a significant clinical challenge in various heart diseases and complications. Although salvianolic acid A (Sal A) from Danshen (Salvia miltiorrhiza) has shown promise in the treatment of ischemic heart disease, myocardial infarction, and atherosclerosis, its effects on cardiac fibrosis remain unexplored. Our study investigated the efficacy of Sal A in reducing cardiac fibrosis and elucidated its underlying molecular mechanisms. We observed that Sal A demonstrated significant cardioprotective effects against Angiotensin II (Ang II)-induced cardiac remodeling and fibrosis, showing a dose-dependent reduction in fibrosis in mice and suppression of cardiac fibroblast proliferation and fibrotic protein expression in vitro. RNA sequencing revealed that Sal A counteracted Ang II-induced upregulation of Txnip, and subsequent experiments indicated that it acts through the inflammasome and ROS pathways. These findings establish the anti-fibrotic effects of Sal A, notably attenuated by Txnip overexpression, and highlight its significant role in modulating inflammation and oxidative stress pathways. This underscores the importance of further research on Sal A and similar compounds, especially regarding their effects on inflammation and oxidative stress, which are key factors in various cardiovascular diseases.

show abstract

Section: Discussionmentioning

confidence: 99%

Salvianolic Acid a Attenuates Angiotensin Ii-Induced Cardiac Fibrosis Through Regulating the Txnip Signaling Pathway

Ye,

Wang,

et al. 2024

Shock

View full text Add to dashboard Cite

show abstract

“…For example, Salvia miltiorrhiza mitigates cardiac dysfunction and inflammation in rats with heart failure by inhibiting the formation of the MD2/TLR4-MyD88 complex [67]. Additionally, Astragaloside IV, Xiang Lin pills, berberine, and fluoxetine can inhibit the TLR4/MyD88/NF-κB signals, thereby exerting the effects of acute myocardial infarction, colitis, and ischemia-reperfusion injury, and relieve postoperative cognitive dysfunction and neuroinflammation in elderly mice [67][68][69][70][71][72][73][74][75][76][77][78][79][80]. Polyene phosphatidylcholine, a wellknown hepatoprotective drug, has also recently been found to act on the TLR2/MyD88 signaling pathway, inhibiting the binding of MyD88 and TLR, and activating the IκB kinase (IKK) complex to alleviate synovial inflammation [81].…”

Section: Drug Therapy Targeting Myd88mentioning

confidence: 99%

MyD88 and Its Inhibitors in Cancer: Prospects and Challenges

Song,

Li,

et al. 2024

Biomolecules

View full text Add to dashboard Cite

The interplay between the immune system and cancer underscores the central role of immunotherapy in cancer treatment. In this context, the innate immune system plays a critical role in preventing tumor invasion. Myeloid differentiation factor 88 (MyD88) is crucial for innate immunity, and activation of MyD88 promotes the production of inflammatory cytokines and induces infiltration, polarization, and immune escape of immune cells in the tumor microenvironment. Additionally, abnormal MyD88 signaling induces tumor cell proliferation and metastasis, which are closely associated with poor prognosis. Therefore, MyD88 could serve as a novel tumor biomarker and is a promising target for cancer therapy. Current strategies targeting MyD88 including inhibition of signaling pathways and protein multimerization, have made substantial progress, especially in inflammatory diseases and chronic inflammation-induced cancers. However, the specific role of MyD88 in regulating tumor immunity and tumorigenic mechanisms remains unclear. Therefore, this review describes the involvement of MyD88 in tumor immune escape and disease therapy. In addition, classical and non-classical MyD88 inhibitors were collated to provide insights into potential cancer treatment strategies. Despite several challenges and complexities, targeting MyD88 is a promising avenue for improving cancer treatment and has the potential to revolutionize patient outcomes.

show abstract

Investigating the NF-κB signaling pathway in heart failure: Exploring potential therapeutic approaches

Ghiasi

2024

Heliyon

View full text Add to dashboard Cite

Salvianolic acid A alleviates heart failure with preserved ejection fraction via regulating TLR/Myd88/TRAF/NF-κB and p38MAPK/CREB signaling pathways

Cited by 11 publications

References 61 publications

Salvianolic Acid a Attenuates Angiotensin Ii-Induced Cardiac Fibrosis Through Regulating the Txnip Signaling Pathway

Salvianolic Acid a Attenuates Angiotensin Ii-Induced Cardiac Fibrosis Through Regulating the Txnip Signaling Pathway

MyD88 and Its Inhibitors in Cancer: Prospects and Challenges

Investigating the NF-κB signaling pathway in heart failure: Exploring potential therapeutic approaches

Contact Info

Product

Resources

About