2011
DOI: 10.1007/s10565-011-9202-x
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Mitigation of H2O2-induced autophagic cell death by propofol in H9c2 cardiomyocytes

Abstract: Autophagy, a self-eating process, is responsible for degradation of long-lived proteins and damaged cellular proteins/organelles. Double-membrane autophagosomes, formed during the process, engulf proteins/organelles and fuse with lysosomes to degrade the contents. It is important to maintain cell homeostasis and many physiological processes including cellular responses to oxidative stress. Oxidative stress induced by myocardial infarction is a major factor of heart failures. In this study, we examined how prop… Show more

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Cited by 30 publications
(21 citation statements)
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“…Six hours after H 2 O 2 challenge, more than 50% cell viability losses were observed in 700 and 900 mM H 2 O 2 H9c2 cells ( P < 0.01 compared with control cells). In parallel, damaged cell morphology was observed using an inverted microscope, shown as broken cellular membranes, swelling, and vacuole degeneration in 700 mM H 2 O 2 treated H9c2 cells (Figure 1(b)), which were quite similar to several previous studies using H9c2 cells [14]. …”
Section: Resultssupporting
confidence: 85%
“…Six hours after H 2 O 2 challenge, more than 50% cell viability losses were observed in 700 and 900 mM H 2 O 2 H9c2 cells ( P < 0.01 compared with control cells). In parallel, damaged cell morphology was observed using an inverted microscope, shown as broken cellular membranes, swelling, and vacuole degeneration in 700 mM H 2 O 2 treated H9c2 cells (Figure 1(b)), which were quite similar to several previous studies using H9c2 cells [14]. …”
Section: Resultssupporting
confidence: 85%
“…2). In contrast, H 2 O 2 at a high concentration (1 mM) increased AMPK phosphorylation in H9c2 cells (18) and adult rat ventricular cardiomyocytes (14).…”
Section: Discussionmentioning
confidence: 89%
“…Generally, activation of extracellular signal-regulated kinases is involved in cardiac cell proliferation and survival 20). On the other hand, Jun N-terminal kinases (JNKs) are activated by several stimuli that induce cardiac myocyte death 21). Recent evidence has implicated the dual role of p38 as a regulator of cell growth, and thus it can promote either cellular survival or death 2).…”
Section: Discussionmentioning
confidence: 99%