ArticleArchives of toxicology2022
Sacubitril/valsartan reduces endoplasmic reticulum stress in a rat model of doxorubicin-induced cardiotoxicity.
Article in Archives of toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- Methylene Blue Mitigates Doxorubicin-Induced Cardiotoxicity via KEAP1/NRF2/GPX-4/Caspase3 Modulation.International journal of molecular sciences · 2025Article
- Vericiguat improves cardiac remodelling and function in rats with doxorubicin-induced cardiomyopathy.ESC heart failure · 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
- Mitigating doxorubicin-induced hepatotoxicity in male rats: The role of aerobic interval training and curcumin supplementation in reducing oxidative stress, endoplasmic reticulum stress and apoptosis.Scientific reports · 2025Article
- Cardioprotective Effects of Dapagliflozin and Trimetazidine on Doxorubicin-Induced Cardiotoxicity in Streptozotocin-Induced Type 1 Diabetic Rats via Endoplasmic Reticulum Stress.Journal of clinical medicine · 2025Article
- Research progress on endoplasmic reticulum homeostasis in acute kidney injury.Frontiers in pharmacology · 2025Review
- Cardiotoxicity caused by acrylamide in rats can be alleviated as a result of suppression of oxidative stress, endoplasmic reticulum stress, inflammation, and apoptosis by morin treatment.Iranian journal of basic medical sciences · 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
- Precision Treatment of Anthracycline-Induced Cardiotoxicity: An Updated Review.Current treatment options in oncology · 2024Review
- Doxorubicin-induced cardiotoxicity and risk factors.International journal of cardiology. Heart & vasculature · 2024Article
- Acute endoplasmic reticulum stress-induced mitochondria respiratory chain damage: The role of activated calpains.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Potential role of endoplasmic reticulum stress in doxorubicin-induced cardiotoxicity-an update.Frontiers in pharmacology · 2024Review
- Synergy effects of copper ion in doxorubicin-based chelate prodrug for cancer chemo-chemodynamic combination therapy.Drug delivery · 2023Article
- Review
- The history and mystery of sacubitril/valsartan: From clinical trial to the real world.Frontiers in cardiovascular medicine · 2023Review
- Endoplasmic reticulum homeostasis: a potential target for diabetic nephropathy.Frontiers in endocrinology · 2023Review
- Tunicamycin-Induced Endoplasmic Reticulum Stress Damages Complex I in Cardiac Mitochondria.Life (Basel, Switzerland) · 2022Article
- Molecular mechanisms of sacubitril/valsartan in cardiac remodeling.Frontiers in pharmacology · 2022Review
- Chemical Chaperones to Inhibit Endoplasmic Reticulum Stress: Implications in Diseases.Drug design, development and therapy · 2022Review
- Effects of Valsartan on LN, FN, MDA, Renal Tissue Fibrosis, and Inflammatory Infiltration in DN Rats.Contrast media & molecular imaging · 2022Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The induction of endoplasmic reticulum (ER) stress has been reported as a key contributor to the cardiotoxicity of doxorubicin. Previous in vitro and in vivo studies suggest that sacubitril/valsartan, a novel angiotensin receptor-neprilysin inhibitor, could be effective against doxorubicin-induced cardiotoxicity. However, the precise mechanisms are not fully understood. Therefore, we investigated whether the cardioprotective effects of sacubitril/valsartan are associated with ER stress modulation in a rat model of doxorubicin-induced cardiotoxicity. Male Sprague-Dawley rats were treated with intraperitoneal injections of doxorubicin (15 mg/kg; cumulative) or saline for 3 weeks. From the day before the first treatment, control animals were gavaged daily with water (n = 8), whereas doxorubicin-treated animals were gavaged daily with water (n = 8) or sacubitril/valsartan (60 mg/kg/day; n = 8) for 6 weeks. Echocardiography was performed 6 weeks after the initiation of doxorubicin. In addition, serum troponin I and N-terminal brain natriuretic peptide levels were determined, and the extent of apoptosis and protein levels related to ER stress in the cardiac tissue and doxorubicin-treated H9c2 cardiomyocytes were analyzed. Sacubitril/valsartan significantly reduced doxorubicin-induced cardiac dysfunction and apoptosis in the myocardium. In addition, sacubitril/valsartan significantly downregulated the expression levels of proteins related to apoptosis and ER stress, including BAX, caspase 3, GRP78, PERK, IRE-1α, ATF-6, eIF-2α, ATF-4, and CHOP, in the myocardium of a rat model of doxorubicin-induced cardiotoxicity in vivo and doxorubicin-treated H9c2 cardiomyocytes in vitro. Sacubitril/valsartan significantly alleviated doxorubicin-induced cardiotoxicity, which may be associated with the reduction of ER stress.
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