Differences in metal content of the heart muscle in death from ischemic heart disease

Chipperfield, Barbara; Chipperfield, J. R.

doi:10.1016/0002-8703(78)90503-3

Cited by 101 publications

(37 citation statements)

References 12 publications

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“…The increased risk of IHD associated with low urinary magnesium excretion complements and extends previous dietary studies showing weak inverse associations (7)(8)(9)(10)12) and autopsy reports of low intracellular magnesium in myocardial tissue after ischemic heart disease (31)(32)(33)(34). Several pathways could explain the beneficial role of magnesium on the heart.…”

Section: Discussionsupporting

confidence: 80%

Urinary and plasma magnesium and risk of ischemic heart disease

Joosten¹,

Gansevoort²,

Mukamal³

et al. 2013

The American Journal of Clinical Nutrition

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Background: Previous studies on dietary magnesium and risk of ischemic heart disease (IHD) have yielded inconsistent results, in part because of a lack of direct measures of actual magnesium uptake. Urinary excretion of magnesium, an indicator of dietary magnesium uptake, might provide more consistent results. Objective: The objective was to investigate whether urinary magnesium excretion and plasma magnesium are associated with IHD risk. Design: We examined 7664 adult participants free of known cardiovascular disease in the Prevention of Renal and Vascular EndStage Disease (PREVEND) study-a prospective population-based cohort study. Urinary magnesium excretion was measured in 2 baseline 24-h urine collections. Results: Mean 6 SD urinary magnesium excretion was 4.24 6 1.65 mmol/24 h for men and 3.54 6 1.40 mmol/24 h for women. During a median follow-up of 10.5 y (IQR: 9.9-10.8 y), 462 fatal and nonfatal IHD events occurred. After multivariable adjustment, urinary magnesium excretion had a nonlinear relation with IHD risk (P-curvature = 0.01). The lowest sex-specific quintile (men: ,2.93 mmol/24 h; women: ,2.45 mmol/24 h) had an increased risk of fatal and nonfatal IHD (multivariable HR: 1.60; 95% CI: 1.28, 2.00) compared with the upper 4 quintiles of urinary magnesium excretion. A similar increase in risk of the lowest quintile was observed for mortality related to IHD (HR: 1.70; 95% CI: 1.10, 2.61). No associations were observed between circulating magnesium and risk of IHD. Conclusions: Low urinary magnesium excretion was independently associated with a higher risk of IHD incidence. An increased dietary intake of magnesium, particularly in those with the lowest urinary magnesium, could reduce the risk of IHD.

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Section: Discussionsupporting

confidence: 80%

Urinary and plasma magnesium and risk of ischemic heart disease

Joosten¹,

Gansevoort²,

Mukamal³

et al. 2013

The American Journal of Clinical Nutrition

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“…For instance, under ischemic or hypertrophic conditions, copper levels in myocardium are significantly reduced (Wester, 1965;Zama and Towns, 1986). The same observation has been found in animal models of ischemic heart disease and pressure overload-induced heart hypertrophy (Chipperfield and Chipperfield, 1978;Chevion et al, 1993;Jiang et al, 2007). It has been shown that under ischemic conditions HIF-1␣ levels increase in the heart (Kim et al, 2002;Su et al, 2002).…”

Section: Downloaded Frommentioning

confidence: 71%

Copper Is Required for Cobalt-Induced Transcriptional Activity of Hypoxia-Inducible Factor-1

Qiu

Ding²,

Zhang³

et al. 2012

J Pharmacol Exp Ther

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Cobalt inhibits prolyl hydroxylases, leading to the accumulation of hypoxia-inducible factor-1␣ (HIF-1␣) and a concomitant increase in the transcriptional activity of HIF-1. Therefore, cobalt has been under development as a drug for activating HIF-1 under some disease conditions. However, it has been shown that ischemic conditions resulted in the loss of copper, and the activation of HIF-1 would not occur unless copper was supplemented. The present study was undertaken to test the hypothesis that copper is also required for the cobalt activation of HIF-1 transcriptional activity. Human umbilical vein endothelial cells subjected to treatment with cobalt chloride (CoCl 2 ) at concentrations above 25 M for 2 h resulted in an accumulation of HIF-1␣, which was determined by Western blot analysis, and an increase in the expression of vascular endothelial growth factor (VEGF), which was determined by real-time reverse transcription-polymerase chain reaction analysis for mRNA levels and enzyme-linked immunosorbent assay analysis for protein levels. The copper chelator tetraethylenepentamine at 25 M did not significantly affect the accumulation of HIF-1␣ but blocked increases in VEGF mRNA and protein levels, an effect that could be reversed by the addition of 25 M copper sulfate (CuSO 4 ). In addition, gene silencing of the copper chaperone for Cu,Zn-superoxide dismutase blocked VEGF expression with little effect on cobalt-induced HIF-1␣ accumulation. The present study thus demonstrates that copper was required for cobalt-activated transcriptional activity of HIF-1, although copper did not affect cobalt-induced accumulation of HIF-1␣ in the cells.

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“…13,14 Necropsy studies of sudden cardiac death victims have revealed that they have a low myocardial Mg content compared with people who died from trauma. 15 Hypomagnesemia is common in intensive care patients, and severe hypomagnesemia has been associated with increased morbidity and mortality in these patients.…”

Section: Discussionmentioning

confidence: 99%