2015
DOI: 10.1016/j.freeradbiomed.2015.09.020
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Novel role of TRPV2 in promoting the cytotoxicity of H2O2-mediated oxidative stress in Human hepatoma cells

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Cited by 26 publications
(23 citation statements)
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“…[6] Study showed that high level of H 2 O 2 could lead to an abundant phosphorylation of p38 in HepG2 and Huh-7 cell lines. [7] Study also highlighted that phosphorylation of p38 MAPK was significantly enhanced in cells under diabetic conditions. [8] The nuclear factor (erythroid-derived 2)-like 2 (Nrf2) plays a protective role against oxidative stress and inflammation.…”
Section: Introductionmentioning
confidence: 88%
See 1 more Smart Citation
“…[6] Study showed that high level of H 2 O 2 could lead to an abundant phosphorylation of p38 in HepG2 and Huh-7 cell lines. [7] Study also highlighted that phosphorylation of p38 MAPK was significantly enhanced in cells under diabetic conditions. [8] The nuclear factor (erythroid-derived 2)-like 2 (Nrf2) plays a protective role against oxidative stress and inflammation.…”
Section: Introductionmentioning
confidence: 88%
“…The phosphorylation and activation of p38 MAPK not only involve in oxidative stress but also play an important role in glucose utilization . Study showed that high level of H 2 O 2 could lead to an abundant phosphorylation of p38 in HepG2 and Huh‐7 cell lines . Study also highlighted that phosphorylation of p38 MAPK was significantly enhanced in cells under diabetic conditions …”
Section: Introductionmentioning
confidence: 99%
“…Also, TRPV1 and TRPV4 were reported to be involved in modulating cell migration . Our previous study suggested that TRPV2 acts as an important enhancer for H 2 O 2 ‐induced cytotoxicity in HepG2 cells . The fact that upregulation of thermo‐TRPVs in ESCC cells prompted us to test their potential role in the development of ESCC.…”
Section: Discussionmentioning
confidence: 97%
“…Interestingly, the expression of TRPV2 mRNA and protein levels in HepG2 and Huh-7 cells was reported to increase upon exposure to ROS, specifically H 2 O 2 , resulting in an activation of cell death. The elevation of TRPV2 expression led to an inhibition of pro-survival signals (Akt, Nrf2) and, in the early stage of apoptosis, promoted the activation of pro-death signals (p38, JNK1) [85]. Another study showed that shRNA-based TRPV2 knockdown in HepG2 cells enhanced spheroid and colony formation, which was restored by the overexpression of TRPV2.…”
Section: Liver Cancermentioning
confidence: 98%