2020
DOI: 10.1080/15376516.2020.1805664
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Oxidative stress-mediated mitochondrial pathway-dependent apoptosis is induced by silica nanoparticles in H9c2 cardiomyocytes

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Cited by 12 publications
(4 citation statements)
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“…Therefore, the suppression of lysosomal proteolysis results in an accumulation of un-degraded vesicles, which leads to increased ROS production and CMs death. 48,52,55 Another pathway that causes DOX-induced cardiotoxic effects is known as ferroptosis. 43 It is characterized by the build-up of iron lipid peroxides, a signicant source of ROS.…”
Section: Discussionmentioning
confidence: 99%
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“…Therefore, the suppression of lysosomal proteolysis results in an accumulation of un-degraded vesicles, which leads to increased ROS production and CMs death. 48,52,55 Another pathway that causes DOX-induced cardiotoxic effects is known as ferroptosis. 43 It is characterized by the build-up of iron lipid peroxides, a signicant source of ROS.…”
Section: Discussionmentioning
confidence: 99%
“…50,51 Patients prescribed DOX are at potential risk of its asymptomatic cardiotoxic side effects, such as elevated stress in the le ventricular wall leading to arrhythmias, heart failure to heart transplantation. 48,55 The principal proposed mechanism of doxorubicin-induced cardiotoxicity is increased oxidative stress. The generation of ROS is the general route by which doxorubicin harms the myocardium.…”
Section: Discussionmentioning
confidence: 99%
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“…Therefore, the increase in the level of ROS in mitochondria is involved in nanoparticle toxicity. [ 42–44 ] Results indicated that inhalation exposure to MWCNTs increased the level of ROS in rat kidney mitochondria. Previous studies also have shown that CNTs can increase the level of ROS.…”
Section: Discussionmentioning
confidence: 99%