ReviewThe American journal of the medical sciences2009
Neurogenic inflammation and cardiac dysfunction due to hypomagnesemia.
Review in The American journal of the medical sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 59 citations in OpenAlex.
- Nutrient insufficiencies and deficiencies involved in the pathogenesis of bruxism (Review).Experimental and therapeutic medicine · 2023Review
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- Understanding How Minerals Contribute to Optimal Immune Function.Journal of immunology research · 2023Review
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- Substance P receptor blocker, aprepitant, inhibited cutaneous and other neurogenic inflammation side effects of the EGFR1-TKI, erlotinib.Molecular and cellular biochemistry · 2020Article
- The role of magnesium in different inflammatory diseases.Inflammopharmacology · 2019Review
- Combination ART-Induced Oxidative/Nitrosative Stress, Neurogenic Inflammation and Cardiac Dysfunction in HIV-1 Transgenic (Tg) Rats: Protection by Mg.International journal of molecular sciences · 2018Article
- Effect of magnesium supplements on serum C-reactive protein: a systematic review and meta-analysis.Archives of medical science : AMS · 2018Review
- Is an Increase in Serum Magnesium One of the Causes of Cardiovascular Events Reduction in the EMPA-REG OUTCOME Study?Journal of clinical medicine research · 2017Article
- EGFR-TKI, erlotinib, causes hypomagnesemia, oxidative stress, and cardiac dysfunction: attenuation by NK-1 receptor blockade.Journal of cardiovascular pharmacology · 2015Article
- Mg supplementation attenuates ritonavir-induced hyperlipidemia, oxidative stress, and cardiac dysfunction in rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- d-Propranolol protects against oxidative stress and progressive cardiac dysfunction in iron overloaded rats.Canadian journal of physiology and pharmacology · 2012Article
- The EGFR tyrosine kinase inhibitor tyrphostin AG-1478 causes hypomagnesemia and cardiac dysfunction.Canadian journal of physiology and pharmacology · 2012Article
- Cation dyshomeostasis and cardiomyocyte necrosis: the Fleckenstein hypothesis revisited.European heart journal · 2011Article
- Mitochondriocentric pathway to cardiomyocyte necrosis in aldosteronism: cardioprotective responses to carvedilol and nebivolol.Journal of cardiovascular pharmacology · 2011Article
- Intra-arterial tert-Butyl-hydroperoxide infusion induces an exacerbated sensory response in the rat hind limb and is associated with an impaired tissue oxygen uptake.Inflammation · 2011Article
- Loss of neutral endopeptidase activity contributes to neutrophil activation and cardiac dysfunction during chronic hypomagnesemia: Protection by substance P receptor blockade.Experimental and clinical cardiology · 2011Article
- The role of magnesium deficiency in cardiovascular and intestinal inflammation.Magnesium research · 2010Article
- Congestive heart failure: where homeostasis begets dyshomeostasis.Journal of cardiovascular pharmacology · 2010Article
- Neutral endopeptidase inhibition enhances substance P mediated inflammation due to hypomagnesemia.Magnesium research · 2009Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Hypomagnesemia continues to be a significant clinical disorder that is present in patients with diabetes mellitus, alcoholism, and treatment with magnesuric drugs (diuretics, cancer chemotherapy agents, etc.). To determine the role of magnesium in cardiovascular pathophysiology, we have used dietary restriction of this cation in animal models. This review highlights some key observations that helped formulate the hypothesis that release of substance P (SP) during experimental dietary Mg deficiency (MgD) may initiate a cascade of deleterious inflammatory, oxidative, and nitrosative events, which ultimately promote cardiomyopathy, in situ cardiac dysfunction, and myocardial intolerance to secondary stresses. SP acts primarily through neurokinin-1 receptors of inflammatory and endothelial cells, and may induce production of reactive oxygen and nitrogen species (superoxide anion, NO*, peroxynitrite, hydroxyl radical), leading to enhanced consumption of tissue antioxidants; stimulate release of inflammatory mediators; promote tissue adhesion molecule expression; and enhance inflammatory cell tissue infiltration and cardiovascular lesion formation. These SP-mediated events may predispose the heart to injury if faced with subsequent oxidative stressors (ischemia/reperfusion, certain drugs) or facilitate development of in situ cardiac dysfunction, especially with prolonged dietary Mg restriction. Significant protection against most of these MgD-mediated events has been observed with interventions that modulate neuronal SP release or its bioactivity, and with several antioxidants (vitamin E, probucol, epicaptopril, d-propranolol). In view of the clinical prevalence of hypomagnesemia, new treatments, beyond magnesium repletion, may be needed to diminish deleterious neurogenic and prooxidative components described in this article.
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