Contrast agent-induced nephrotoxicity: role of oxidative stress and apoptosis through the mitochondrial pathway

Stewart, Joanna D.; Hengstler, Jan G.; Bolt, Hermann M.

doi:10.1007/s00204-011-0666-5

Cited by 10 publications

(5 citation statements)

References 14 publications

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“…In another study, specific inhibitors of caspase-3 and -9 attenuated the CM-induced injury of LLC-PK1 cells, while specific inhibitors of caspase-8 did not (28), indicating that contrast-induced apoptosis occurs primarily through the mitochondrial pathway. In the present study, the expression levels of various apoptosis-associated proteins were investigated, demonstrating that the expression of caspase-3 and c-caspase-9 were markedly higher following iohexol treatment, compared with the blank group, which supports previous findings (24)(25)(26). However, no significant differences were observed in the expression levels of caspase-9 between the two groups.…”

Section: Discussionsupporting

confidence: 89%

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Role of TLR4/MyD88/NF‑κB signaling in the contrast‑induced injury of renal tubular epithelial cells

et al. 2020

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The aim of the present study was to explore the role of toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88)/nuclear factor (NF)-κB signaling in the contrast-induced injury of renal tubular epithelial cells, and to investigate the potential mechanisms. HK-2 cells cultured in vitro were randomly divided into six groups as follows: i) The blank group; ii) the iohexol group; iii) the NF-κB RNAi group (NF-κB siRNA + iohexol); iv) the TLR4 RNAi group (TLR4 siRNA + iohexol); v) the NF-κB blocker group (PDTC + iohexol); and vi) the TLR4 blocker group (CLI-095 + iohexol). The expression of the TLR4/MyD88/NF-κB signaling pathway proteins was detected by reverse transcription-quantitative (RT-q)PCR and western blot analysis, and the cellular proliferation rate was determined using the Cell Counting Kit-8 assay. The mRNA expression levels of the inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were also detected using RT-qPCR, and apoptosis was assessed by flow cytometry and western blotting to detect apoptosis-associated proteins (caspase-3, caspase-9 and cleaved caspase-9). Compared with the blank group, the apoptotic rates and the expression levels of TLR4, MyD88, NF-κB, caspase-3, cleaved caspase-9, TNF-α, IL-1β and IL-6 were upregulated in the iohexol group (P<0.001). However, when TLR4 or NF-κB were blocked or silenced, these effects were reversed (P<0.001). Collectively, the results of the present study indicated that TLR4/MyD88/NF-κB signaling is involved in the contrast-induced injury of renal tubular epithelial cells by inducing inflammation and apoptosis.

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Section: Discussionsupporting

confidence: 89%

“…In CIN, caspase-9 is activated through the mitochondrial pathway, which subsequently activates the downstream caspase-3 and induces apoptosis (26). Previous studies have demonstrated that, in hypotonic or isotonic CM-induced in vitro models, caspase-9 and -3 were activated, while caspase-8 and -10 were not (27).…”

Section: Discussionmentioning

confidence: 99%

Role of TLR4/MyD88/NF‑κB signaling in the contrast‑induced injury of renal tubular epithelial cells

et al. 2020

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“…Several factors have been reported to be associated with the pathogenesis of CIN, including the CIN risk factor evaluation including hypotension, intra-aortic balloon pump, congestive heart failure, age of >75 years, anemia, diabetes mellitus, contrast dosage, baseline creatinine and creatinine clearance rate, as well as the combination of diabetes mellitus and renal insufficiency. [ 11 , 17 , 18 ] Serum Cys-C level after coronary angiography could reflect the changes of serum eGFR, while its sensitivity was superior to the serum Scr as Scr was affected by several factors such as age, sex, and diets. Previously, Wang et al [ 19 ] showed that CIN pathogenesis was associated with age, female individuals, contrast dosage, and exposure time.…”

Section: Discussionmentioning

confidence: 99%

Association between plasma endothelial microparticles and contrast-induced nephropathy in patients underwent coronary angiography

Dong

Wang

et al. 2021

Medicine

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We aim to investigate the association between plasma endothelial microparticles (EMPs) and contrast-induced nephropathy of patients underwent coronary angiography. The patients were divided into normal renal function group and renal dysfunction group based on the estimated glomerular filtration rate (eGFR). Among the 180 cases, 117 received determination of EMP and serum creatinine after percutaneous coronary intervention (PCI) and/or coronary angiography. The patients were divided into contrast-induced-nephropathy (CIN) group and non-CIN group. EMPs collection and determination were performed, together with biochemical analysis and digital subtraction angiography (DSA) analysis. Spearman correlation showed that the expression of EMP was negatively correlated with eGFR ( r = –0.201, P < .01). The serum hypersensitive C-reactive protein (hs-CRP), cystatin C (Cys-C), uric acid (UA) were significantly higher in CIN group than that in the non CIN group. Spearman correlation showed that the expression of EMP was positively correlated with serum interleukin-6 (IL-6, r = 0.393, P < .01). The expression of EMP was positively correlated with serum hs-CRP ( r = 0.360, P < .01). Logistic regression analysis showed that the levels of N-terminal pro-brain natriuretic peptide (NT-proBNP), eGFR, UA, and Cys-C were correlated with the incidence of contrast induced nephropathy. In patients with contrast-induced-nephropathy, the plasma EMPs were significantly increased after coronary angiography. The expression of plasma EMPs may play a role in the occurrence of contrast-induced-nephropathy.

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“…A special focus of the review of Chasapis et al (2011;this issue) is the role of zinc in apoptosis, which is particularly welcome, since the control mechanisms of apoptosis is critical for the fields of toxicology and cancer research (Lee et al 2010(Lee et al , 2011Kirsch-Volders et al 2011;Yen et al 2011;Wang et al 2011;Fang et al 2011;Cheng et al 2011;Golka et al 2011;Kunwar et al 2011;Baird and DinkovaKostova 2011;Sun et al 2011;Stewart et al 2011;Zhao et al 2011;Park et al 2011;El Hakim et al 2011;Ilowski et al 2011;Godoy et al 2009Godoy et al , 2010Petry et al 2010;Franke et al 2009;Hardelauf et al 2011;Cadenas et al 2010). Zinc is a known inhibitor of apoptosis.…”

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confidence: 99%

Zinc as a multipurpose trace element

2012

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Contrast agent-induced nephrotoxicity: role of oxidative stress and apoptosis through the mitochondrial pathway

Cited by 10 publications

References 14 publications

Role of TLR4/MyD88/NF‑κB signaling in the contrast‑induced injury of renal tubular epithelial cells

Role of TLR4/MyD88/NF‑κB signaling in the contrast‑induced injury of renal tubular epithelial cells

Association between plasma endothelial microparticles and contrast-induced nephropathy in patients underwent coronary angiography

Zinc as a multipurpose trace element

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Contrast agent-induced nephrotoxicity: role of oxidative stress and apoptosis through the mitochondrial pathway

Cited by 10 publications

References 14 publications

Role of TLR4/MyD88/NF‑&kappa;B signaling in the contrast‑induced injury of renal tubular epithelial cells

Role of TLR4/MyD88/NF‑&kappa;B signaling in the contrast‑induced injury of renal tubular epithelial cells

Association between plasma endothelial microparticles and contrast-induced nephropathy in patients underwent coronary angiography

Zinc as a multipurpose trace element

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Role of TLR4/MyD88/NF‑κB signaling in the contrast‑induced injury of renal tubular epithelial cells

Role of TLR4/MyD88/NF‑κB signaling in the contrast‑induced injury of renal tubular epithelial cells