Search Results - "Imamoto, Toru"

Dichloroacetate reduces cisplatin-induced apoptosis by inhibiting the JNK/14-3-3/Bax/caspase-9 pathway and suppressing caspase-8 activation via cFLIP in murine tubular cells by Kimura, Hideki, Kamiyama, Kazuko, Imamoto, Toru, Takeda, Izumi, Kobayashi, Mamiko, Takahashi, Naoki, Kasuno, Kenji, Sugaya, Takeshi, Iwano, Masayuki

“…Cisplatin-induced injury to renal proximal tubular cells stems from mitochondrial damage-induced apoptosis and inflammation. Dichloroacetate (DCA), a pyruvate…”
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PPAR-δ activation reduces cisplatin-induced apoptosis via inhibiting p53/Bax/caspase-3 pathway without modulating autophagy in murine renal proximal tubular cells by Shan, Juanping, Kimura, Hideki, Yokoi, Seiji, Kamiyama, Kazuko, Imamoto, Toru, Takeda, Izumi, Kobayashi, Mamiko, Mikami, Daisuke, Takahashi, Naoki, Kasuno, Kenji, Sugaya, Takeshi, Iwano, Masayuki

“…Background Cisplatin-induced injury of renal proximal tubular cells results basically from increased apoptosis via mitochondrial damage, and is mitigated by…”
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PPAR-α Insufficiency Enhances Doxorubicin-Induced Nephropathy in PPAR-α Knockout Mice and a Murine Podocyte Cell Line by Matsuta, Kohei, Kamiyama, Kazuko, Imamoto, Toru, Takeda, Izumi, Masunaga, Shinya, Kobayashi, Mamiko, Takahashi, Naoki, Kasuno, Kenji, Hara, Masanori, Iwano, Masayuki, Toyama, Tadashi, Kimura, Hideki

“…Peroxisome proliferator-activated receptor-alpha (PPAR-α) and its exogenous activators (fibrates) promote autophagy. However, whether the deleterious effects…”
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Fenofibrate reduces cisplatin-induced apoptosis by inhibiting the p53/Puma/Caspase-9 pathway and the MAPK/Caspase-8 pathway rather than by promoting autophagy in murine renal proximal tubular cells by Kimura, Hideki, Kamiyama, Kazuko, Imamoto, Toru, Takeda, Izumi, Masunaga, Shinya, Kobayashi, Mamiko, Mikami, Daisuke, Takahashi, Naoki, Kasuno, Kenji, Sugaya, Takeshi, Iwano, Masayuki

“…The main lesion of cisplatin nephrotoxicity is damage to proximal tubular cells due to increased apoptosis via the mitochondrial and death receptor pathways,…”
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