ArticleFrontiers in pharmacology2022
A Novel Compound, Tanshinol Borneol Ester, Ameliorates Pressure Overload-Induced Cardiac Hypertrophy by Inhibiting Oxidative Stress via the mTOR/β-TrCP/NRF2 Pathway.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Poge heart-saving decoction meliorates heart failure by suppressing apoptosis and fibrosis via regulation of the PI3K/AKT pathway.Frontiers in pharmacology · 2026Article
- Model organisms for investigating the functional involvement of NRF2 in non-communicable diseases.Redox biology · 2025Review
- Enhancing Cardioprotection Through Neutrophil-Mediated Delivery of 18β-Glycyrrhetinic Acid in Myocardial Ischemia/Reperfusion Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- HAPLN1 knockdown inhibits heart failure development via activating the PKA signaling pathway.BMC cardiovascular disorders · 2024Article
- Neutrophil membrane-camouflaged nanoparticles alleviate inflammation and promote angiogenesis in ischemic myocardial injury.Bioactive materials · 2023Article
- High Glucose-Induced Cardiomyocyte Damage Involves Interplay between Endothelin ET-1/ETInternational journal of molecular sciences · 2022Article
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tanshinol borneol ester (DBZ) exerts anti-atherosclerotic and anti-inflammatory effects. However, its effects on cardiac hypertrophy are not well understood. In this work, we investigated the treatment effects and potential mechanisms of DBZ on the hypertrophic heart under oxidative stress and endoplasmic reticulum (ER) stress. A hypertrophic model was established in rats using transverse-aortic constriction (TAC) surgery and in neonatal rat cardiomyocytes (NRCMs) using angiotensin II (Ang II). Our results revealed that DBZ remarkably inhibited oxidative stress and ER stress, blocked autophagy flow, and decreased apoptosis
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