SLC41A2遺伝子欠損マウスのアドリアマイシン腎症の重篤化

• 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
• Language: Japanese
• Published: 公益社団法人 日本薬理学会 2020
• Subjects: magnesium; transporter
• ISSN: 2435-4953
• DOI: 10.1254/jpssuppl.93.0_2-P-239

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.