Vitamin K: Redox-modulation, prevention of mitochondrial dysfunction and anticancer effect

Ivanova, Donika; Zhelev, Zhivko; Getsov, Plamen; Nikolova, Biliana; Aoki, Ichio; Higashi, Tatsuya; Bakalova, Rumiana

doi:10.1016/j.redox.2018.03.013

Cited by 99 publications

(75 citation statements)

References 89 publications

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“…In nature, plant forms (vitamin K1 and phylloquinone) and bacterial forms (vitamin K2 and menaquinones) are the isoprenologs of vitamin K. After being ingested from the intestine, vitamin K is transported to the liver with triacylglycerol-rich lipoprotein, where vitamin K1 is transformed into vitamin K2 [41]. The transformed vitamin K2 is transported to extrahepatic tissues, such as bones, arteries, and macrophages, by low-density lipoproteins [42]. In extrahepatic tissue, menaquinone-4 is the major form of vitamin K with a mode of action.…”

Section: Introductionmentioning

confidence: 99%

Emerging Role of Vitamins D and K in Modulating Uremic Vascular Calcification: The Aspect of Passive Calcification

Hou

Zheng

et al. 2019

Nutrients

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Vascular calcification is a critical complication in patients with chronic kidney disease (CKD) because it is predictive of cardiovascular events and mortality. In addition to the traditional mechanisms associated with endothelial dysfunction and the osteoblastic transformation of vascular smooth muscle cells (VSMCs), the regulation of calcification inhibitors, such as calciprotein particles (CPPs) and matrix vesicles plays a vital role in uremic vascular calcification in CKD patients because of the high prevalence of vitamin K deficiency. Vitamin K governs the gamma-carboxylation of matrix Gla protein (MGP) for inhibiting vascular calcification, and the vitamin D binding protein receptor is related to vitamin K gene expression. For patients with chronic kidney disease, adequate use of vitamin D supplements may play a role in vascular calcification through modulation of the calciprotein particles and matrix vesicles (MVs).

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Section: Introductionmentioning

confidence: 99%

Emerging Role of Vitamins D and K in Modulating Uremic Vascular Calcification: The Aspect of Passive Calcification

Hou

Zheng

et al. 2019

Nutrients

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“…It has also been shown that mitochondria function normally even in glycolysis-dependent cancer cells, and that glutamine metabolism and FAO are activated [ 50 , 51 , 52 , 54 , 55 ]. In vitro and in vivo experiments have shown that inhibitors of mitochondrial OXPHOS, such as metformin, phenformin, and menadione, suppress CSC traits [ 132 , 163 , 164 , 165 , 166 , 167 ]. Also, since mitochondria are derived from a prokaryote that originally parasitized eukaryotic cells, it is known that its function can be inhibited by treatment with various antibiotics [ 17 , 18 , 19 , 20 , 168 , 169 , 170 ].…”

Section: Therapeutic Strategies For Targeting Csc Metabolismmentioning

confidence: 99%

The Metabolic Heterogeneity and Flexibility of Cancer Stem Cells

Tanabe

Sahara

2020

Cancers

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Numerous findings have indicated that CSCs, which are present at a low frequency inside primary tumors, are the main cause of therapy resistance and cancer recurrence. Although various therapeutic methods targeting CSCs have been attempted for eliminating cancer cells completely, the complicated characteristics of CSCs have hampered such attempts. In analyzing the biological properties of CSCs, it was revealed that CSCs have a peculiar metabolism that is distinct from non-CSCs to maintain their stemness properties. The CSC metabolism involves not only the catabolic and anabolic pathways, but also intracellular signaling, gene expression, and redox balance. In addition, CSCs can reprogram their metabolism to flexibly respond to environmental changes. In this review, we focus on the flexible metabolic mechanisms of CSCs, and highlight the new therapeutics that target CSC metabolism.

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“…Antioxidants compound targeted to reduce ROS and increase antioxidant enzymes that result in protection against ischemic injury. Moreover, there is evidence that overexpression of antioxidant enzymes can reduce oxidative stress in oxygen-glucose-deprived neurons and global cerebral ischemia [101,102]. Although Vitamin K is not known as a classical antioxidant, research reports that Vitamin K1 and K2 (menaquinone-4) potently inhibit glutathione depletion-mediated oxidative cell death.…”

Section: Plos Onementioning

confidence: 99%

Neuroprotective effect of menaquinone-4 (MK-4) on transient global cerebral ischemia/reperfusion injury in rat

Moghadam

Fereidoni

2020

PLoS ONE

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Cerebral ischemia/reperfusion (I/R) injury causes cognitive deficits, excitotoxicity, neuroinflammation, oxidative stress and brain edema. Vitamin K2 (Menaquinone 4, MK-4) as a potent antioxidant can be a good candidate to ameliorate I/R consequences. This study focused on the neuroprotective effects of MK-4 for cerebral I/R insult in rat's hippocampus. The rat model of cerebral I/R was generated by transient bilateral common carotid artery occlusion for 20 min. Rats were divided into control, I/R, I/R+DMSO (solvent (1% v/ v)) and I/R+MK-4 treated (400 mg/kg, i.p.) groups. Twenty-four hours after I/R injury induction, total brain water content, superoxide dismutase (SOD) activity, nitrate/nitrite concentration and neuronal density were evaluated. In addition to quantify the apoptosis processes, TUNEL staining, as well as expression level of Bax and Bcl2, were assessed. To evaluate astrogliosis and induced neurotoxicity by I/R GFAP and GLT-1 mRNA expression level were quantified. Furthermore, pro-inflammatory cytokines including IL-1β, IL-6 and TNF-α were measured. Seven days post I/R, behavioral analysis to quantify cognitive function, as well as Nissl staining for surviving neuronal evaluation, were conducted. The findings indicated that administration of MK-4 following I/R injury improved anxiety-like behavior, short term and spatial learning and memory impairment induced by I/R. Also, MK-4 was able to diminish the increased total brain water content, apoptotic cell density, Bax/ Bcl2 ratio and GFAP mRNA expression following I/R. In addition, the high level of nitrate/nitrite, IL-6, IL-1β and TNF-α induced by I/R was reduced after MK-4 administration. However, MK-4 promotes the level of SOD activity and GLT-1 mRNA expression in I/R rat model. The findings demonstrated that MK-4 can rescue transient global cerebral I/R consequences via its anti-inflammatory and anti-oxidative stress features. MK-4 administration ameliorates neuroinflammation, neurotoxicity and neuronal cell death processes and leads to neuroprotection. PLOS ONEPLOS ONE | https://doi.org/10.1371/journal.pone.0229769 March 9, 2020 1 / 30 OPEN ACCESS Citation: Farhadi Moghadam B, Fereidoni M (2020) Neuroprotective effect of menaquinone-4 (MK-4) on transient global cerebral ischemia/reperfusion injury in rat. PLoS ONE 15(3): e0229769. https://

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Vitamin K: Redox-modulation, prevention of mitochondrial dysfunction and anticancer effect

Cited by 99 publications

References 89 publications

Emerging Role of Vitamins D and K in Modulating Uremic Vascular Calcification: The Aspect of Passive Calcification

Emerging Role of Vitamins D and K in Modulating Uremic Vascular Calcification: The Aspect of Passive Calcification

The Metabolic Heterogeneity and Flexibility of Cancer Stem Cells

Neuroprotective effect of menaquinone-4 (MK-4) on transient global cerebral ischemia/reperfusion injury in rat

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