Magnesium in renal fibrosis

Long, Mengtuan; Zhu, Xiaoyu; Wei, Xuejiao; Zhao, Dan; Jiang, Lili; Li, Chenhao; Jin, Die; Miao, Changxiu; Du, Yujun

doi:10.1007/s11255-022-03118-3

Cited by 8 publications

(5 citation statements)

References 85 publications

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“…AGE-increased NADPH oxidase activity upregulates intracellular ROS ( 252 ). Consequently, ROS may activate the NF-kB pathway and MAPK recruitment, resulting in the release of cytokines and chemokines ( 254 , 255 ). Mg 2+ is suggested to reduce apoptosis by diminishing MAPK and NF-kB signaling ( 255 ).…”

Section: Potential Molecular Mechanisms Of Magnesium Involvement In C...mentioning

confidence: 99%

“…Consequently, ROS may activate the NF-kB pathway and MAPK recruitment, resulting in the release of cytokines and chemokines ( 254 , 255 ). Mg 2+ is suggested to reduce apoptosis by diminishing MAPK and NF-kB signaling ( 255 ). Thus, hypomagnesemia may lead to increased AGE levels, as well as downstream signaling of MAPKs and NF-kB ( 251 ).…”

Section: Potential Molecular Mechanisms Of Magnesium Involvement In C...mentioning

confidence: 99%

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Hypomagnesemia and Cardiovascular Risk in Type 2 Diabetes

2022

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Hypomagnesemia is tenfold more common in individuals with type 2 diabetes (T2D), compared to the healthy population. Factors that are involved in this high prevalence are low Mg2+ intake, gut microbiome composition, medication use and presumably genetics. Hypomagnesemia is associated with insulin resistance, which subsequently increases the risk to develop T2D or deteriorates glycaemic control in existing diabetes. Mg2+ supplementation decreases T2D associated features like dyslipidaemia and inflammation; which are important risk factors for cardiovascular disease (CVD). Epidemiological studies have shown an inverse association between serum Mg2+ and the risk to develop heart failure (HF), atrial fibrillation (AF) and microvascular disease in T2D. The potential protective effect of Mg2+ on HF and AF may be explained by reduced oxidative stress, fibrosis and electrical remodeling in the heart. In microvascular disease, Mg2+ reduces the detrimental effects of hyperglycemia and improves endothelial dysfunction. Though, clinical studies assessing the effect of long-term Mg2+ supplementation on CVD incidents are lacking and gaps remain on how Mg2+ may reduce CVD risk in T2D. Despite the high prevalence of hypomagnesemia in people with T2D, routine screening of Mg2+ deficiency to provide Mg2+ supplementation when needed is not implemented in clinical care as sufficient clinical evidence is lacking. In conclusion, hypomagnesemia is common in people with T2D and is both involved as cause, probably through molecular mechanisms leading to insulin resistance, and consequence and is prospectively associated with development of HF, AF and microvascular complications. Whether long-term supplementation of Mg2+ is beneficial, however, remains to be determined.

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Section: Potential Molecular Mechanisms Of Magnesium Involvement In C...mentioning

confidence: 99%

Section: Potential Molecular Mechanisms Of Magnesium Involvement In C...mentioning

confidence: 99%

Hypomagnesemia and Cardiovascular Risk in Type 2 Diabetes

2022

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“…Disturbances in the concentration of the two biometals are involved in the pathogenesis of numerous diseases [2][3][4][5] and influence the action of some drugs [6,7] .…”

Section: Introductionmentioning

confidence: 99%

Interactions of Antibacterial Antibiotics with Magnesium and Zinc

Nechifor,

Luca,

Gales

2024

ijirms

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The action of antibacterial antibiotics on bacteria but also on the cells of the human body is dependent on many factors. An important place is the interactions with magnesium and zinc. The aim of this narrative review is to highlight the complexity of interactions between these two cations and some antibacterial antibiotics. The review presents pharmacokinetic, pharmacodynamic interactions and the influence of magnesium and zinc on some adverse effects of antibiotics. The influences of some antibiotics on plasma concentrations of magnesium and zinc are also discussed. The interactions take place before the contact of the antibiotic with the pathogenic bacteria, during the action on bacteria but also after this action. Some adverse effects of antibiotics are produced by their direct action on human cells and plasma and tissue concentrations of magnesium and zinc are important for reducing these effects. These two biometals play multiple and complex roles in the human body. Some antibiotics such as aminoglycosides and polymyxins greatly increase the renal excretion of magnesium and significantly decrease the plasma concentration of this cation. Zinc increases the bacterial sensitivity to the action of beta-lactams. The polymerization of vancomycin dimers increases the antibacterial activity and it is dependent of zinc. Zinc oxide nanoparticles have a significant antibiofilm action. On the other hand, magnesium and zinc salts greatly reduce the digestive absorption of many antibiotics and decrease their bioavailability. Regarding adverse effects, there are situations were magnesium and zinc can reduce some of these effects. A low magnesium level aggravates the cartilage damage produced by quinolones. This cation reduces nephrotoxicity of Aminoglycosides and vancomycin and hepatotoxicity of some antituberculosis drugs. Determination of zinc and magnesium concentration is strictly necessary for patients receiving antibiotics and in the case of abnormal levels, correction must be made immediately.

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“…Given that peritoneal calcification in PD patients is caused by persistent peritoneal exposure to a high-Ca, high-phosphate environment, Mg may be able to prevent peritoneal calcification in the later stage of EPS. Mg has also been shown to retard inflammation-driven renal and lung fibrosis 10 , 11 . Considering the underlying pathology of EPS, intraperitoneal Mg supplementation may be an effective treatment option for patients at heightened risk of EPS.…”

Section: Introductionmentioning

confidence: 99%

Magnesium inhibits peritoneal calcification as a late-stage characteristic of encapsulating peritoneal sclerosis

Aihara,

Yamada,

Matsueda

et al. 2023

Sci Rep

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Peritoneal calcification is a prominent feature of the later stage of encapsulating peritoneal sclerosis (EPS) in patients undergoing long-term peritoneal dialysis (PD). However, the pathogenesis and preventive strategy for peritoneal calcification remain unclear. Peritoneum samples from EPS patients were examined histologically. Peritoneal calcification was induced in mice by feeding with an adenine-containing diet combined with intraperitoneal administration of lipopolysaccharide and a calcifying solution containing high calcium and phosphate. Excised mouse peritoneum, human mesothelial cells (MeT5A), and mouse embryonic fibroblasts (MEFs) were cultured in calcifying medium. Immunohistochemistry confirmed the appearance of osteoblastic differentiation-marker-positive cells in the visceral peritoneum from EPS patients. Intraperitoneal administration of magnesium suppressed peritoneal fibrosis and calcification in mice. Calcifying medium increased the calcification of cultured mouse peritoneum, which was prevented by magnesium. Calcification of the extracellular matrix was accelerated in Met5A cells and MEFs treated with calcification medium. Calcifying medium also upregulated osteoblastic differentiation markers in MeT5A cells and induced apoptosis in MEFs. Conversely, magnesium supplementation mitigated extracellular matrix calcification and phenotypic transdifferentiation and apoptosis caused by calcifying conditions in cultured MeT5A cells and MEFs. Phosphate loading contributes to the progression of EPS through peritoneal calcification and fibrosis, which can be prevented by magnesium supplementation.

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Magnesium in renal fibrosis

Cited by 8 publications

References 85 publications

Hypomagnesemia and Cardiovascular Risk in Type 2 Diabetes

Hypomagnesemia and Cardiovascular Risk in Type 2 Diabetes

Interactions of Antibacterial Antibiotics with Magnesium and Zinc

Magnesium inhibits peritoneal calcification as a late-stage characteristic of encapsulating peritoneal sclerosis

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