Wolf Federica I, Trapani Valentina, Cittadini Achille
Istituto di Patologia generale e Centro di Ricerche Oncologiche Giovanni XXIII, Università Cattolica del Sacro Cuore, Facoltà di Medicina A. Gemelli, 00168 Roma, Italy.
Magnes Res. 2008 Jun;21(2):83-91.
Experimental evidence supports the important role of magnesium in the process of cellular proliferation, even though cell magnesium homeostasis is not completely clarified. We were the first to describe some molecular characteristics of the magnesium-dependent regulation of the cell cycle, and others proposed a mechanism for the magnesium-dependent regulation of protein synthesis occurring in the early phases of cell proliferation. We will attempt to relate such mechanisms with pathologic conditions whereby cell proliferation is severely disregulated, as in the case of tumors. It is interesting to note that recently some efforts have been made to correlate magnesium transport systems with its functions within the cells. Few, but stimulating new data are emerging which relate molecularly defined ion channels with magnesium homeostasis and its functions. Old and new data are now being merged and corroborated by diverse experimental approaches including molecular genetics, proteomics, electrophysiology and biochemistry. This, together with the development of new techniques to measure cell magnesium content and distribution, will hopefully pave the way to unravel the intimate mechanisms of such an essential though undefined metabolic regulator. New and deeper appreciation of magnesium homeostasis will help in delineating the key role of this cation in the regulation of normal or pathologic cell proliferation.
实验证据支持镁在细胞增殖过程中的重要作用，尽管细胞镁稳态尚未完全阐明。我们是第一个描述细胞周期镁依赖性调节的一些分子特征的，其他人则提出了细胞增殖早期发生的蛋白质合成镁依赖性调节机制。我们将尝试将这些机制与细胞增殖严重失调的病理状况联系起来，比如肿瘤的情况。值得注意的是，最近已经做出了一些努力，将镁转运系统与其在细胞内的功能联系起来。出现了一些虽少但很有启发性的新数据，这些数据将分子定义的离子通道与镁稳态及其功能联系起来。现在，新旧数据正通过包括分子遗传学、蛋白质组学、电生理学和生物化学在内的多种实验方法进行整合和验证。这一点，再加上测量细胞镁含量和分布的新技术的发展，有望为揭示这种虽至关重要但尚不明确的代谢调节因子的内在机制铺平道路。对镁稳态有更新、更深入的认识将有助于阐明这种阳离子在调节正常或病理细胞增殖中的关键作用。
