Modulation of Cardiac Ion Channels by Magnesium

Agus, Zalman S.; Morad, Martin

doi:10.1146/annurev.ph.53.030191.001503

Cited by 144 publications

(56 citation statements)

References 19 publications

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“…It had been reported that an excess amount of intracellular Mg 2ϩ induced by hyperactivity of N-methyl-D-aspartate channels occasionally causes neuronal cell death as a result of inhibitory effects of Mg 2ϩ to mitochondrial activities (24). The change of [Mg 2ϩ ] i in OGD/CI may also affect the cellular function in which magnesium is required as follows: maintenance of the active conformation of macromolecules, regulation of lipid-and phosphoinositide-derived second messengers, regulation of transporters and ion channels (33,54), etc.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia Induces an Increase in Intracellular Magnesium via Transient Receptor Potential Melastatin 7 (TRPM7) Channels in Rat Hippocampal Neurons in Vitro

Zhang¹,

Zhao²,

Zhao

et al. 2011

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Hypoxia Induces an Increase in Intracellular Magnesium via Transient Receptor Potential Melastatin 7 (TRPM7) Channels in Rat Hippocampal Neurons in Vitro

Zhang¹,

Zhao²,

Zhao

et al. 2011

Journal of Biological Chemistry

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“…Interestingly, several direct myocardial effects of magnesium have been demonstrated. (14) Thus, it is possible that magnesium may confer cardio-protective effects. Given that HF is associated with high morbidity and mortality 2 and imposes a significant economic burden on health systems, it is therefore necessary to further evaluate putative risk factors which may have predictive or causal relevance to the risk of HF and which could help tailor preventive and therapeutic interventions.…”

Section: Introductionmentioning

confidence: 99%

Serum magnesium and risk of new onset heart failure in men: the Kuopio Ischemic Heart Disease Study

2016

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Link to publication record in Explore Bristol Research PDF-document This is the author accepted manuscript (AAM). The final published version (version of record) is available online via Springer at http://link.springer.com/article/10.1007/s10654-016-0164-4. Please refer to any applicable terms of use of the publisher. University of Bristol -Explore Bristol Research General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Full terms of use are available: http://www.bristol.ac.uk/pure/about/ebr-terms AbstractSerum magnesium is an essential intracellular cation involved in processes that regulate cardiovascular function and has been linked to the risk of several cardiovascular disease outcomes. We aimed to investigate the association of serum magnesium concentrations with risk of incident heart failure (HF). We studied 2,181 middle-aged men without prevalent HF (aged 42-61 years) enrolled in the Finnish Kuopio Ischemic Heart Disease prospective cohort study with serum magnesium measurements made at baseline.Hazard ratios (95% confidence intervals [CI]) for HF were assessed. During a median follow-up of 24.8 years, 278 HF events occurred. Baseline serum magnesium was weakly and inversely associated with several clinical markers and was continuously associated with risk of HF. The age-adjusted HR (95% CIs) for HF per 1 standard deviation (SD) higher serum magnesium levels was 0.86 (0.76-0.97). The HR (95% CIs) was 0.87 (0.76-0.98) after controlling for measures of adiposity, socio-economic variables, medical history, blood pressure, renal function, alcohol consumption, and lipids. These findings remained consistent in analyses accounting for incident coronary heart disease. The results were comparable across several clinically relevant subgroups and analyses with atrial fibrillation as a competing risk yielded similar results. Serum magnesium was continuously, inversely and independently associated with future risk of HF. Further research is needed to assess any potential relevance of serum magnesium in HF prevention.

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“…As the most abundant divalent cation in mammalian cells [3], intracellular magnesium plays a crucial role in numerous cellular functions in cardiac cells, including the enzyme activities and the gating of ion channels [4,5]. By regulating cell growth and proliferation, Mg 2+ could facilitate the vascular remodeling and fibrosis, the characteristic features of vascular damage in hypertension, atherosclerosis and diabetes [6].…”

Section: Introductionmentioning

confidence: 99%

SLC41A1 knockdown inhibits angiotensin II-induced cardiac fibrosis by preventing Mg2+ efflux and Ca2+ signaling in cardiac fibroblasts

Jiang

et al. 2014

Archives of Biochemistry and Biophysics

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Modulation of Cardiac Ion Channels by Magnesium

Cited by 144 publications

References 19 publications

Hypoxia Induces an Increase in Intracellular Magnesium via Transient Receptor Potential Melastatin 7 (TRPM7) Channels in Rat Hippocampal Neurons in Vitro

Hypoxia Induces an Increase in Intracellular Magnesium via Transient Receptor Potential Melastatin 7 (TRPM7) Channels in Rat Hippocampal Neurons in Vitro

Serum magnesium and risk of new onset heart failure in men: the Kuopio Ischemic Heart Disease Study

SLC41A1 knockdown inhibits angiotensin II-induced cardiac fibrosis by preventing Mg2+ efflux and Ca2+ signaling in cardiac fibroblasts

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