Curcumin attenuates bevacizumab-induced toxicity via suppressing oxidative stress and preventing mitochondrial dysfunction in heart mitochondria

Sabet, Nima Shokouhi; Atashbar, Saman; Khanlou, Elham Mohammad; Kahrizi, Farzad; Salimi, Ahmad

doi:10.1007/s00210-020-01853-x

Cited by 31 publications

(17 citation statements)

References 50 publications

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“…Doxorubicin induces oxidative stress, resulting in the production of a great deal of ROS ( Sheibani et al, 2020 ) which changes the permeability of mitochondria ( Kaludercic and Di Lisa, 2020 ). The formation of disulfide bonds around the mitochondrial permeability transition pore (MPTP) or MPT leads to the opening of the mitochondrial MPT pore ( Sabet et al, 2020 ) and ROS can induce the opening of the MPT pore ( Kaludercic and Di Lisa, 2020 ). Once opened, the metabolites and ions in the MPT pore dissipate grads, proton power collapses, resulting in the rupture of the outer membrane of the mitochondria and the swelling of a large number of mitochondria ( Sabet et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

“…The formation of disulfide bonds around the mitochondrial permeability transition pore (MPTP) or MPT leads to the opening of the mitochondrial MPT pore ( Sabet et al, 2020 ) and ROS can induce the opening of the MPT pore ( Kaludercic and Di Lisa, 2020 ). Once opened, the metabolites and ions in the MPT pore dissipate grads, proton power collapses, resulting in the rupture of the outer membrane of the mitochondria and the swelling of a large number of mitochondria ( Sabet et al, 2020 ). The opening of MPT leads to the release of apoptosis factors (such as cytochrome C)from the mitochondria to the cytoplasm and initiates the endogenous mitochondrial apoptosis pathway ( Morciano et al, 2015 ).…”

Section: Discussionmentioning

confidence: 99%

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aFGF Targeted Mediated by Novel Nanoparticles-Microbubble Complex Combined With Ultrasound-Targeted Microbubble Destruction attenuates Doxorubicin-Induced Heart Failure via Anti-Apoptosis and Promoting Cardiac Angiogenesis

et al. 2021

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The purpose of this study was to evaluate the protective effect of acidic fibroblast growth factor targeted mediated by novel nanoparticles–cationic lipid microbubbles complex (aFGF–NP + CPMBs) combined with ultrasound targeted microbubble destruction (UTMD)on doxorubicin–induced heart failure (HF)and its mechanism. Heart failure rats induced by intraperitoneal injection with doxorubicin (DOX) to achieve cummulative dose of 15mg/kg for continuous 6 weeks showed left ventricular dysfunction, seriously oxidative stress, cardiomyocyte apoptosis, and decrease of myocardial vascular density. In contrast, aFGF–NP + CPMBs combined with UTMD therapy (3ug/kg, caudal vein injection, twice a week, 6weeks)prominently ameliorated left ventricular dysfunction by increased ejection fraction (EF) and fractional shortening (FS), decreased brain natriuretic peptide (BNP); strengthened the ability of antioxidant stress confirmed by increasing the activity of SOD and reducing the production of MDA; exerted the effect of anti–cardiomyocyte apoptosis and promotion angiogenesis by inhibited Bax expression and increased Bcl–2 expression and platelet endothelial cell adhesion molecule (CD31) expression. Taken together, the research suggested that aFGF targeted mediated by novel nanoparticles–cationic lipid microbubbles complex combined with UTMD should be a promising targeted treatment for heart failure.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

aFGF Targeted Mediated by Novel Nanoparticles-Microbubble Complex Combined With Ultrasound-Targeted Microbubble Destruction attenuates Doxorubicin-Induced Heart Failure via Anti-Apoptosis and Promoting Cardiac Angiogenesis

et al. 2021

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“…Bevacizumab was the first anti-VEGF antibody with a rate of sytemic hypertension as high as 70%, probably because of the vascular resistance, endothelial dysfunction, and capillary rarefection (39). Bevacizumab induces mitochondrial dysfunction plus ROS formation in isolated rat heart (60,61) and in isolated cardiomyocytes (62).…”

Section: Anti-vascular Endothelial Growth Factor (Vegf) Monoclonal An...mentioning

confidence: 99%

New Insights in Early Detection of Anticancer Drug-Related Cardiotoxicity Using Perfusion and Metabolic Imaging

Cadour

Thuny

Sourdon

2022

Front. Cardiovasc. Med.

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Cardio-oncology requires a good knowledge of the cardiotoxicity of anticancer drugs, their mechanisms, and their diagnosis for better management. Anthracyclines, anti-vascular endothelial growth factor (VEGF), alkylating agents, antimetabolites, anti-human epidermal growth factor receptor (HER), and receptor tyrosine kinase inhibitors (RTKi) are therapeutics whose cardiotoxicity involves several mechanisms at the cellular and subcellular levels. Current guidelines for anticancer drugs cardiotoxicity are essentially based on monitoring left ventricle ejection fraction (LVEF). However, knowledge of microvascular and metabolic dysfunction allows for better imaging assessment before overt LVEF impairment. Early detection of anticancer drug-related cardiotoxicity would therefore advance the prevention and patient care. In this review, we provide a comprehensive overview of the cardiotoxic effects of anticancer drugs and describe myocardial perfusion, metabolic, and mitochondrial function imaging approaches to detect them before over LVEF impairment.

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“…Mitochondria are highly dynamic organelles that fuse and divide continuously, adjusting their cellular distribution according to the energy demands of the cell. Several mitochondrial proteins are involved in fusion and fission events, including mitofusins 1 and 2 (MFN1, MFN2), optic atrophy 1 protein (OPA-1), dynamin-related protein (DRP1), and fission 1 (FIS1) [28]. Among these, MFN1, MFN2, and OPA-1 are involved in mitochondrial fusion, while DRP1 is required for mitochondrial fission [29].…”

Section: Role Of Phbs In Mitochondrial Biogenesismentioning

confidence: 99%

Prohibitins: A Key Link between Mitochondria and Nervous System Diseases

Jiang

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Prohibitins (PHBs) are conserved proteins in eukaryotic cells, which are mainly located in the inner mitochondrial membrane (IMM), cell nucleus, and cell membrane. PHBs play crucial roles in various cellular functions, including the cell cycle regulation, tumor suppression, immunoglobulin M receptor binding, and aging. In addition, recent in vitro and in vivo studies have revealed that PHBs are important in nervous system diseases. PHBs can prevent apoptosis, inflammation, mitochondrial dysfunction, and autophagy in neurological disorders through different molecules and pathways, such as OPA-1, PINK1/Parkin, IL6/STAT3, Tau, NO, LC3, and TDP43. Therefore, PHBs show great promise in the protection of neurological disorders. This review summarizes the relevant studies on the relationship between PHBs and neurological disorders and provides an update on the molecular mechanisms of PHBs in nervous system diseases.

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Curcumin attenuates bevacizumab-induced toxicity via suppressing oxidative stress and preventing mitochondrial dysfunction in heart mitochondria

Cited by 31 publications

References 50 publications

aFGF Targeted Mediated by Novel Nanoparticles-Microbubble Complex Combined With Ultrasound-Targeted Microbubble Destruction attenuates Doxorubicin-Induced Heart Failure via Anti-Apoptosis and Promoting Cardiac Angiogenesis

aFGF Targeted Mediated by Novel Nanoparticles-Microbubble Complex Combined With Ultrasound-Targeted Microbubble Destruction attenuates Doxorubicin-Induced Heart Failure via Anti-Apoptosis and Promoting Cardiac Angiogenesis

New Insights in Early Detection of Anticancer Drug-Related Cardiotoxicity Using Perfusion and Metabolic Imaging

Prohibitins: A Key Link between Mitochondria and Nervous System Diseases

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