SLC41A2遺伝子欠損マウスのアドリアマイシン腎症の重篤化

Mg2+ is an essential divalent cation, which plays pivotal roles in fundamental cellular functions. Mg2+ deficiency or abnormal Mg2+ metabolism is related to various cardiovascular and neuromuscular diseases. In recent years, several candidate genes of Mg2+ transporters including SLC41A1/A2 have been...

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Published in日本薬理学会年会要旨集 p. 2-P-239
Main Authors 根本, 隆行, 田頭, 秀章, 喜多, 知, 喜多, 紗斗美, 岩本, 隆宏
Format Journal Article
LanguageJapanese
Published 公益社団法人 日本薬理学会 2020
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Summary:Mg2+ is an essential divalent cation, which plays pivotal roles in fundamental cellular functions. Mg2+ deficiency or abnormal Mg2+ metabolism is related to various cardiovascular and neuromuscular diseases. In recent years, several candidate genes of Mg2+ transporters including SLC41A1/A2 have been reported. We have been studying their physiological roles and pathological significances using genetic altered mice targeting each candidate gene. Recently, we generated and characterized SLC41A1/A2 mice, and found that these mice exhibited dysregulation of serum Mg2+ levels and urinary Mg2+ excretion. Here we show that adriamycin-induced nephropathy (albuminuria, renal glomerular degeneration) was markedly aggravated in SLC41A2 knockout mice, but not in SLC41A1 knockout mice, compared to wild-type mice. On the other hand, cisplatin-induced nephrotoxicity was observed to the similar degree among SLC41A1/A2 knockout mice and wild-type mice.These results suggest that SLC41A2 is involved in the development and progression of adriamycin-induced nephropathy.
Bibliography:93_2-P-239
ISSN:2435-4953
DOI:10.1254/jpssuppl.93.0_2-P-239