The role of selenium in bevacizumab induced cardiotoxicity

Öncel, Can Ramazan

doi:10.4149/bll_2019_021

Cited by 4 publications

(4 citation statements)

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“…Lung cancer or thoracic cancers are frequently managed with immunotherapy, radiation, chemotherapy as monotherapy, or radiation combined with chemotherapeutic agents, such as platinum (cisplatin and carboplatin), microtubule inhibitors taxanes (docetaxel and paclitaxel), blood vessel formation inhibitors (bevacizumab), epidermal growth factor inhibitors (erlotinib and necitumumab), and immunotherapies [ 23 ] (nivolumab, pembrolizumab, atezolizumab, and ipilimumab). Cancer therapeutics cause cardiopulmonary toxicities including hypertension and myocardial ischemia [ 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 ], and this is accepted by the American Cancer Society and American Heart Association. According to the US National Cancer Institute (NCI) and based on our previous knowledge, chemotherapy or immunotherapy promote toxicity/inflammation in non-target organs and these inflammations invite migration of neutrophils, macrophages, and cytotoxic lymphocytes to injured and non-injured sites [ 6 ].…”

Section: Cancer Therapy-induced Inflammation and Cardiopulmonary Fibrosismentioning

confidence: 99%

Dark Side of Cancer Therapy: Cancer Treatment-Induced Cardiopulmonary Inflammation, Fibrosis, and Immune Modulation

Boopathi

Thangavel

2021

IJMS

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Advancements in cancer therapy increased the cancer free survival rates and reduced the malignant related deaths. Therapeutic options for patients with thoracic cancers include surgical intervention and the application of chemotherapy with ionizing radiation. Despite these advances, cancer therapy-related cardiopulmonary dysfunction (CTRCPD) is one of the most undesirable side effects of cancer therapy and leads to limitations to cancer treatment. Chemoradiation therapy or immunotherapy promote acute and chronic cardiopulmonary damage by inducing reactive oxygen species, DNA damage, inflammation, fibrosis, deregulation of cellular immunity, cardiopulmonary failure, and non-malignant related deaths among cancer-free patients who received cancer therapy. CTRCPD is a complex entity with multiple factors involved in this pathogenesis. Although the mechanisms of cancer therapy-induced toxicities are multifactorial, damage to the cardiac and pulmonary tissue as well as subsequent fibrosis and organ failure seem to be the underlying events. The available biomarkers and treatment options are not sufficient and efficient to detect cancer therapy-induced early asymptomatic cell fate cardiopulmonary toxicity. Therefore, application of cutting-edge multi-omics technology, such us whole-exome sequencing, DNA methylation, whole-genome sequencing, metabolomics, protein mass spectrometry and single cell transcriptomics, and 10 X spatial genomics, are warranted to identify early and late toxicity, inflammation-induced carcinogenesis response biomarkers, and cancer relapse response biomarkers. In this review, we summarize the current state of knowledge on cancer therapy-induced cardiopulmonary complications and our current understanding of the pathological and molecular consequences of cancer therapy-induced cardiopulmonary fibrosis, inflammation, immune suppression, and tumor recurrence, and possible treatment options for cancer therapy-induced cardiopulmonary toxicity.

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Section: Cancer Therapy-induced Inflammation and Cardiopulmonary Fibrosismentioning

confidence: 99%

Dark Side of Cancer Therapy: Cancer Treatment-Induced Cardiopulmonary Inflammation, Fibrosis, and Immune Modulation

Boopathi

Thangavel

2021

IJMS

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“…In addition, high serum troponin I (TP I) and creatine kinase MB (CK‐MB) levels were found in BVZ‐treated rats 6 . Moreover, studies have shown that human cardiomyocytes treated with BVZ exhibited increased cytosolic calcium, apoptosis, and reactive oxygen species (ROS) production 7 . However, the intracellular molecular mechanisms underlying BVZ‐associated cardiotoxicity have yet to be fully understood.…”

Section: Introductionmentioning

confidence: 99%

“… 6 Moreover, studies have shown that human cardiomyocytes treated with BVZ exhibited increased cytosolic calcium, apoptosis, and reactive oxygen species (ROS) production. 7 However, the intracellular molecular mechanisms underlying BVZ‐associated cardiotoxicity have yet to be fully understood. A previous study reported that VEGFA was involved in BVZ‐induced cardiomyocyte toxicity.…”

Section: Introductionmentioning

confidence: 99%

Interferon‐regulatory factor‐1 boosts bevacizumab cardiotoxicity by the vascular endothelial growth factor A/14‐3‐3γ axis

Chen,

Xie,

Huang

et al. 2024

ESC Heart Failure

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AimMyocardial injury is a significant cause of death. This study investigated the role and underlying mechanism of interferon‐regulatory factor‐1 (IRF1) in bevacizumab (BVZ)‐induced cardiomyocyte injury.Methods and resultsHL‐1 cells and C57BL/6 mice receiving BVZ treatment were used to establish in vitro and in vivo models of myocardial injury. The relationship between VEGFA and 14‐3‐3γ was verified through co‐immunoprecipitation and Glutathione S Transferase (GST) pull‐down assay. Cell viability and apoptosis were analysed by MTT, propidium iodide (PI) staining and flow cytometry. The release of lactate dehydrogenase (LDH), cardiac troponins T (cTnT), and creatine kinase MB (CK‐MB) was measured using the enzyme linked immunosorbent assay. The effects of knocking down IRF1 on BVZ‐induced mice were analysed in vivo. IRF1 levels were increased in BVZ‐treated HL‐1 cells. BVZ treatment induced apoptosis, inhibited cell viability, and promoted the release of LDH, cTnT, and CK‐MB. IRF1 silencing suppressed BVZ‐induced myocardial injury, whereas IRF1 overexpression had the opposite effect. IRF1 regulated VEGFA expression by binding to its promoter, with the depletion of VEGFA or 14‐3‐3γ reversing the effects of IRF1 knockdown on the cell viability and apoptosis of BVZ‐treated HL‐1 cells. 14‐3‐3γ overexpression promoted cell proliferation, inhibited apoptosis, and reduced the release of LDH, cTnT, and CK‐MB, thereby alleviating BVZ‐induced HL‐1 cell damage. In vivo, IRF1 silencing alleviated BVZ‐induced cardiomyocyte injury by regulating the VEGFA/14‐3‐3γ axis.ConclusionThe IRF1‐mediated VEGFA/14‐3‐3γ signalling pathway promotes BVZ‐induced myocardial injury. Our study provides evidence for potentially new target genes for the treatment of myocardial injury.

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“…Hyperglycemia and hyperlipidemia lead to mitochondria dysfunction which causes cellular energy depletion and reactive oxygen species (ROS) generation and finally results in hepatocellular apoptosis and death (Gouaref et al 2017;Tilg et al 2017). Previous studies demonstrated that the transient receptor potential receptor vanilloid 1 (TRPV1) is a mechanosensitive ion channel that has been shown to regulate the energy expenditure and cholesterol metabolism in hepatocytes (Wang et al 2013;Harb et al 2019), while activation of TRPV1 has been identified to protect against stresses induced oxidative toxicity in various cells such as neuronal cells (Ataizi and Ertilav 2020), cardiomyocytes (Oncel and Ovey 2019), human umbilical artery smooth muscle cells (Schwartz et al 2018) and bone marrow-derived macrophages (Yan et al 2019). Therefore, we infer that TRPV1 could modulate redox signals to prevent high glucose-and high fatty-acid-intake-induced liver injury.…”

Section: Introductionmentioning

confidence: 99%

TRPV1 Protect against Hyperglycemia and Hyperlipidemia Induced Liver Injury via OPA1 in Diabetes

Wang¹,

Chen²,

Li³

et al. 2022

Tohoku J. Exp. Med.

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Type 2 diabetes mellitus (T2DM)-associated mitochondrial impairment may a key factor leading to liver injury. Transient receptor potential receptor vanilloid 1 (TRPV1) regulates the energy expenditure and cholesterol metabolism in hepatocytes and protects against oxidative toxicity. Optic atrophy 1 (OPA1) is involved in the protection of TRPV1 on cardiac microvascular and lung injury. The aim of this study is to identify the role of TRPV1 in redox signals and liver protection via OPA1. TRPV1 knockout (TRPV1 -/-) mice were used. And T2DM associated liver injury was induced by high glucose and high fatty acid (HG/HF) treatment. Mechanisms were studied by TUNEL staining, transmission electron microscope (TEM) analysis, reverse transcription polymerase chain reaction (RT-PCR) and Western blotting in vivo and in vitro. We determined that HG/HF treatment increased TRPV1 expression in liver tissues and AML12 cells. The knockout of TRPV1 increased the apoptotic hepatocytes rate. The inhibition of TRPV1 by 5'-iRTX in HG/HF group elevated the reactive oxygen species (ROS) levels, whereas TRPV1 agonist capsaicin reduced ROS. Our studies also showed that the OPA1 expression was lower in livers from HG/HF treated mice than the control, and genetic ablation of TRPV1 decreased OPA1 expression to a greater extent than the HG/HF mice. The protective effects of TRPV1 on mitochondrial were blocked by OPA1 siRNA. In conclusion, our study showed that the identified regulation of TRPV1 to OPA1 has important implication to the pathogenesis of T2DM-associated liver injury. Targeting the action of TRPV1 and OPA1 presents a potential therapeutic intervention.

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The role of selenium in bevacizumab induced cardiotoxicity

Cited by 4 publications

References 50 publications

Dark Side of Cancer Therapy: Cancer Treatment-Induced Cardiopulmonary Inflammation, Fibrosis, and Immune Modulation

Dark Side of Cancer Therapy: Cancer Treatment-Induced Cardiopulmonary Inflammation, Fibrosis, and Immune Modulation

Interferon‐regulatory factor‐1 boosts bevacizumab cardiotoxicity by the vascular endothelial growth factor A/14‐3‐3γ axis

TRPV1 Protect against Hyperglycemia and Hyperlipidemia Induced Liver Injury via OPA1 in Diabetes

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