Sacubitril/valsartan reduces endoplasmic reticulum stress in a rat model of doxorubicin-induced cardiotoxicity

Kim, Byung Sik; Park, In-Hwa; Lee, A-Hyeon; Kim, Hyun‐Jin; Lim, Young‐Hyo; Shin, Jeong‐Hun

doi:10.1007/s00204-022-03241-1

Cited by 28 publications

(13 citation statements)

References 37 publications

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“…MEK is an upstream kinase of ERK and can participate in the process of ERK entry into the nucleus. The MEK-specific inhibitor U0126 can inhibit the MEK/ERK pathway and thus inhibit the migration of cavity squamous cell carcinoma [ 16 ]. Nrf1, as a mitochondrial function gene, can regulate antioxidant genes, proteasome genes, and other transcription genes, so as to play an antioxidative stress role and protect cells from oxidative stress [ 17 ].…”

Section: Related Workmentioning

confidence: 99%

[Retracted] Effects of Valsartan on LN, FN, MDA, Renal Tissue Fibrosis, and Inflammatory Infiltration in DN Rats

Qin¹,

Li²,

Chen

et al. 2022

Contrast Media & Molecular Imaging

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The effects of valsartan on laminin (LN), fibronectin (FN), malondialdehyde (MDA), renal tissue fibrosis, and inflammatory infiltration in diabetic nephropathy (DN) rats are explored. A total of 42 SPF male Sprague D (SD) rats are selected and randomly divided into normal set, model set, valsartan low-dose and high-dose sets, and metformin set with 7 rats in each set. The kidney tissue of all rats is collected after administration. The standard of protein mRNA in kidney tissues is detected by real-time fluorescence quantitative polymerase chain reaction (PCR) method, and the protein standard in kidney tissues is detected by western blot. The experimental results show that the application of valsartan to DN rats can effectively relieve the morphology of the rat kidney tissue, enhance the protein expression in the kidney tissue of the DN rats, and reduce the fibrosis and inflammatory infiltration of the kidney tissue.

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Section: Related Workmentioning

confidence: 99%

[Retracted] Effects of Valsartan on LN, FN, MDA, Renal Tissue Fibrosis, and Inflammatory Infiltration in DN Rats

Qin¹,

Li²,

Chen

et al. 2022

Contrast Media & Molecular Imaging

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“…ER stress occurs in many pathological conditions including aging [ 28 , 29 , 30 ], diabetic disease [ 24 ], doxorubicin cardiotoxicity [ 31 ], and heart failure [ 27 ]. Attenuation of the ER stress leads to improved mitochondrial function in aged hearts, indicating that the ER stress contributes to mitochondrial dysfunction during aging [ 28 , 29 , 30 ].…”

Section: Introductionmentioning

confidence: 99%

Tunicamycin-Induced Endoplasmic Reticulum Stress Damages Complex I in Cardiac Mitochondria

Chen¹,

Thompson²,

Hu³

et al. 2022

Life

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Background: Induction of acute ER (endoplasmic reticulum) stress using thapsigargin contributes to complex I damage in mouse hearts. Thapsigargin impairs complex I by increasing mitochondrial calcium through inhibition of Ca2+-ATPase in the ER. Tunicamycin (TUNI) is used to induce ER stress by inhibiting protein folding. We asked if TUNI-induced ER stress led to complex I damage. Methods: TUNI (0.4 mg/kg) was used to induce ER stress in C57BL/6 mice. Cardiac mitochondria were isolated after 24 or 72 h following TUNI treatment for mitochondrial functional analysis. Results: ER stress was only increased in mice following 72 h of TUNI treatment. TUNI treatment decreased oxidative phosphorylation with complex I substrates compared to vehicle with a decrease in complex I activity. The contents of complex I subunits including NBUPL and NDUFS7 were decreased in TUNI-treated mice. TUNI treatment activated both cytosolic and mitochondrial calpain 1. Our results indicate that TUNI-induced ER stress damages complex I through degradation of its subunits including NDUFS7. Conclusion: Induction of the ER stress using TUNI contributes to complex I damage by activating calpain 1.

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“…Furthermore, endoplasmic reticulum stress (ERS) was one of the key pathogenesis of doxorubicin-related heart failure. Sacubitril/valsartan markedly improved doxorubicinrelated cardiac dysfunction by downregulating the protein expression associated with ERS and apoptosis in a rat model (36).…”

Section: Animal Experimental Modelsmentioning

confidence: 93%

Cancer treatment-related cardiotoxicity: A focus on sacubitril/valsartan

hu¹,

et al. 2022

Preprint

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Cardiotoxicity is the most dramatic complications of cancer therapies, leading to halt in potentially life-saving anti-tumor treatment regimens and a poor survival prognosis in a non-negligible percentage of patients. Angiotensin converting enzyme inhibitors (ACEIs) and β-blockers are effective in the treatment of the cancer therapy–related cardiac dysfunction (CTRCD), while their roles in the prevention of cardiotoxicity are unclear. Sacubitril/valsartan was advantageous over ACEI in heart failure patients for further reduction of cardiovascular death or heart failure re-hospitalization. However, there is short of well-established testimony of its efficacy and safety in the prevention and treatment of CTRCD in the cardio-oncology setting. Although some small observational studies found a good performance of sacubitril/valsartan in patients with CTRCD, large-scale prospective clinical studies are required to confirm its excellent results. In this paper, we review the potential benefit of sacubitril/valsartan in human subjects with CTRCD.

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Sacubitril/valsartan reduces endoplasmic reticulum stress in a rat model of doxorubicin-induced cardiotoxicity

Cited by 28 publications

References 37 publications

[Retracted] Effects of Valsartan on LN, FN, MDA, Renal Tissue Fibrosis, and Inflammatory Infiltration in DN Rats

[Retracted] Effects of Valsartan on LN, FN, MDA, Renal Tissue Fibrosis, and Inflammatory Infiltration in DN Rats

Tunicamycin-Induced Endoplasmic Reticulum Stress Damages Complex I in Cardiac Mitochondria

Cancer treatment-related cardiotoxicity: A focus on sacubitril/valsartan

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