ArticleScientific reports2022
LCZ696 ameliorates doxorubicin-induced cardiomyocyte toxicity in rats.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Cardiac drug potential: exploring individual and combined cardiac drugs to promote differentiation of adipose-derived stem cells into cardiomyocytes.Molecular biology reports · 2026Article
- Angiotensin receptor-neprilysin inhibitors improve the outcome of lung cancer patients with hypertension undergoing immune checkpoint inhibitors treatment.BMC cardiovascular disorders · 2025Article
- Thymoquinone chemically conjugated to doxorubicin: antitumor activity and subcellular localization.RSC advances · 2025Article
- Sacubitril/valsartan attenuated myocardial inflammation, fibrosis, apoptosis and promoted autophagy in doxorubicin-induced cardiotoxicity mice via regulating the AMPKα-mTORC1 signaling pathway.Molecular and cellular biochemistry · 2025Article
- Value of Label-Free Ubiquitin-Proteomic Analysis on Defining the Protective Mechanism of Valsartan against Doxorubicin-Induced Heart Failure.Current cancer drug targets · 2025Article
- Sacubitril/Valsartan Combination Partially Improves Cardiac Systolic, but Not Diastolic, Function through β-AR Responsiveness in a Rat Model of Type 2 Diabetes.International journal of molecular sciences · 2024Article
- Role of Oxidative Stress and Inflammation in Doxorubicin-Induced Cardiotoxicity: A Brief Account.International journal of molecular sciences · 2024Review
- Doxorubicin-induced cardiotoxicity and risk factors.International journal of cardiology. Heart & vasculature · 2024Article
- Ferroptosis-induced Cardiotoxicity and Antitumor Drugs.Current medicinal chemistry · 2024Review
- Utilization of QuinceACS omega · 2023Article
- Sacubitril/Valsartan Ameliorates Crizotinib-Induced Cardiotoxicity in Mice.Reviews in cardiovascular medicine · 2023Article
- Review
- Targeting mitochondrial dynamics proteins for the treatment of doxorubicin-induced cardiotoxicity.Frontiers in molecular biosciences · 2023Review
- The Role of NF-κB and Bax/Bcl-2/Caspase-3 Signaling Pathways in the Protective Effects of Sacubitril/Valsartan (Entresto) against HFD/STZ-Induced Diabetic Kidney Disease.Biomedicines · 2022Article
- LCZ696 Ameliorates Isoproterenol-Induced Acute Heart Failure in Rats by Activating the Nrf2 Signaling Pathway.Applied bionics and biomechanics · 2022Article
- Molecular mechanisms of sacubitril/valsartan in cardiac remodeling.Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (DOX)-based chemotherapy induces cardiotoxicity, which is considered the main bottleneck for its clinical application. In this study, we investigated the potential benefit of LCZ696, an angiotensin receptor-neprilysin inhibitor against DOX-induced cardiotoxicity in rats and H9c2 cells and determined whether the mechanism underlying any such effects involves its antioxidant activity. Male Sprague-Dawley rats were randomly separated into four groups, each consisting of 15 rats (DOX (1.5 mg/kg/day intraperitoneally for 10 days followed by non-treatment for 8 days); DOX + valsartan (31 mg/kg/day by gavage from day 1 to day 18); DOX + LCZ696 (68 mg/kg/day by gavage from day 1 to day 18); and control (saline intraperitoneally for 10 days). DOX-induced elevation of cardiac troponin T levels on day 18 was significantly reduced by LCZ696, but not valsartan. The DOX-induced increase in myocardial reactive oxygen species (ROS) levels determined using dihydroethidium was significantly ameliorated by LCZ696, but not valsartan, and was accompanied by the suppression of DOX-induced increase in p47phox. LCZ696 recovered the DOX-induced decrease in phosphorylation of adenosine monophosphate-activated protein kinase and increased the ratio of Bax and Bcl-2. In H9c2 cardiomyocytes, LCZ696 reduced DOX-induced mitochondrial ROS generation and improved cell viability more than valsartan. Our findings indicated that LCZ696 ameliorated DOX-induced cardiotoxicity in rat hearts in vivo and in vitro, possibly by mediating a decrease in oxidative stress.
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