Beyond Ion Homeostasis: Hypomagnesemia, Transient Receptor Potential Melastatin Channel 7, Mitochondrial Function, and Inflammation.
Beyond Ion Homeostasis: Hypomagnesemia, Transient Receptor Potential Melastatin Channel 7, Mitochondrial Function, and Inflammation.
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DOI：
10.3390/nu15183920
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发表时间：
2023-09-09
期刊：
影响因子：
5.9
通讯作者：
Dudley SC Jr
中科院分区：
文献类型：
--
作者：
Liu M;Dudley SC Jr
作为细胞内第二丰富的二价阳离子，镁（Mg²⁺）对细胞功能至关重要，例如三磷酸腺苷（ATP）的产生、蛋白质/脱氧核糖核酸（DNA）合成、蛋白质活性以及线粒体功能。Mg²⁺在心律、肌肉收缩和血压方面起着关键作用。据报道，由于加工食品和过滤/去离子水的消费量增加，发达国家的Mg²⁺摄入量显著下降，这可能导致低镁血症（HypoMg）。低镁血症常见于心血管疾病，如心力衰竭、高血压、心律失常和糖尿病性心肌病，并且是心血管疾病和全因死亡率的一个预测因素。另一方面，补充Mg²⁺在心血管疾病中已显示出显著的治疗效果。低镁血症的一些影响归因于Mg²⁺参与酶活性、ATP稳定、酶动力学以及Ca²⁺、Na⁺和其他阳离子的改变。在本文中，我们讨论对低镁血症致病机制的新见解，这些见解超越了先前描述的影响。低镁血症导致线粒体功能障碍、氧化应激和炎症。许多这些影响可归因于低镁血症诱导的一种Mg²⁺转运体——瞬时受体电位 melastatin 7通道（TRMP7，它也是一种激酶）的上调。由低镁血症诱导的TRPM7转录上调所介导的激酶信号增加，与Mg²⁺转运功能的任何改变无关，似乎很可能是低镁血症的许多影响的原因。因此，补充Mg²⁺和抑制TRPM7激酶可能通过防止TRPM7激酶活性增加而非仅仅改变离子稳态来治疗低镁血症的后遗症。由于许多疾病以氧化应激或炎症为特征，补充Mg²⁺和抑制TRPM7激酶可能通过减轻氧化应激和炎症对其他疾病有更广泛的影响。
As the second most abundant intracellular divalent cation, magnesium (Mg2+) is essential for cell functions, such as ATP production, protein/DNA synthesis, protein activity, and mitochondrial function. Mg2+ plays a critical role in heart rhythm, muscle contraction, and blood pressure. A significant decline in Mg2+ intake has been reported in developed countries because of the increased consumption of processed food and filtered/deionized water, which can lead to hypomagnesemia (HypoMg). HypoMg is commonly observed in cardiovascular diseases, such as heart failure, hypertension, arrhythmias, and diabetic cardiomyopathy, and HypoMg is a predictor for cardiovascular and all-cause mortality. On the other hand, Mg2+ supplementation has shown significant therapeutic effects in cardiovascular diseases. Some of the effects of HypoMg have been ascribed to changes in Mg2+ participation in enzyme activity, ATP stabilization, enzyme kinetics, and alterations in Ca2+, Na+, and other cations. In this manuscript, we discuss new insights into the pathogenic mechanisms of HypoMg that surpass previously described effects. HypoMg causes mitochondrial dysfunction, oxidative stress, and inflammation. Many of these effects can be attributed to the HypoMg-induced upregulation of a Mg2+ transporter transient receptor potential melastatin 7 channel (TRMP7) that is also a kinase. An increase in kinase signaling mediated by HypoMg-induced TRPM7 transcriptional upregulation, independently of any change in Mg2+ transport function, likely seems responsible for many of the effects of HypoMg. Therefore, Mg2+ supplementation and TRPM7 kinase inhibition may work to treat the sequelae of HypoMg by preventing increased TRPM7 kinase activity rather than just altering ion homeostasis. Since many diseases are characterized by oxidative stress or inflammation, Mg2+ supplementation and TRPM7 kinase inhibition may have wider implications for other diseases by acting to reduce oxidative stress and inflammation.
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影响因子：
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作者：
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DOI：
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发表时间：
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影响因子：
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