Vitamin K2 (MK-7) attenuates LPS-induced acute lung injury via inhibiting inflammation, apoptosis, and ferroptosis

Wang, Yulian; Yang, Weidong; Liu, Lulu; Liu, Lihong; Chen, Jiepeng; Duan, Lili; Li, Yuyuan; Li, Shuzhuang

doi:10.1371/journal.pone.0294763

Cited by 4 publications

(3 citation statements)

References 64 publications

(69 reference statements)

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“…Recent animal research has demonstrated that vitamin K2 is a potential therapeutic option for acute lung injury. It may alleviate acute lung injury by regulating inflammation, apoptosis, ferroptosis, and elastin degradation [ 98 ]. This may be due to the longer half-life of vitamin K2 [ 66 ].…”

Section: Resultsmentioning

confidence: 99%

Vitamin K: a potential missing link in critical illness–a scoping review

Paulus,

Drent,

Kouw

et al. 2024

Crit Care

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Background Vitamin K is essential for numerous physiological processes, including coagulation, bone metabolism, tissue calcification, and antioxidant activity. Deficiency, prevalent in critically ill ICU patients, impacts coagulation and increases the risk of bleeding and other complications. This review aims to elucidate the metabolism of vitamin K in the context of critical illness and identify a potential therapeutic approach. Methods In December 2023, a scoping review was conducted using the PRISMA Extension for Scoping Reviews. Literature was searched in PubMed, Embase, and Cochrane databases without restrictions. Inclusion criteria were studies on adult ICU patients discussing vitamin K deficiency and/or supplementation. Results A total of 1712 articles were screened, and 13 met the inclusion criteria. Vitamin K deficiency in ICU patients is linked to malnutrition, impaired absorption, antibiotic use, increased turnover, and genetic factors. Observational studies show higher PIVKA-II levels in ICU patients, indicating reduced vitamin K status. Risk factors include inadequate intake, disrupted absorption, and increased physiological demands. Supplementation studies suggest vitamin K can improve status but not normalize it completely. Vitamin K deficiency may correlate with prolonged ICU stays, mechanical ventilation, and increased mortality. Factors such as genetic polymorphisms and disrupted microbiomes also contribute to deficiency, underscoring the need for individualized nutritional strategies and further research on optimal supplementation dosages and administration routes. Conclusions Addressing vitamin K deficiency in ICU patients is crucial for mitigating risks associated with critical illness, yet optimal management strategies require further investigation. Impact research To the best of our knowledge, this review is the first to address the prevalence and progression of vitamin K deficiency in critically ill patients. It guides clinicians in diagnosing and managing vitamin K deficiency in intensive care and suggests practical strategies for supplementing vitamin K in critically ill patients. This review provides a comprehensive overview of the existing literature, and serves as a valuable resource for clinicians, researchers, and policymakers in critical care medicine.

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Section: Resultsmentioning

confidence: 99%

Vitamin K: a potential missing link in critical illness–a scoping review

Paulus,

Drent,

Kouw

et al. 2024

Crit Care

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“…In a previous study [ 63 ], we also carried out some protective studies of vitamin K2 on acute lung injury. The conclusions of the two articles are consistent, both of which reflected the fact that vitamin K2 can protect ALI mice by interfering with inflammation and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Vitamin K2 (MK-7) on Acute Lung Injury Induced by Lipopolysaccharide in Mice

Yang,

Wang,

Liu

et al. 2024

CIMB

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Vitamin K2 (MK-7) has been shown to cause significant changes in different physiological processes and diseases, but its role in acute lung injury (ALI) is unclear. Therefore, in this study, we aimed to evaluate the protective effects of VK2 against LPS-induced ALI in mice. The male C57BL/6J mice were randomly divided into six groups (n = 7): the control group, LPS group, negative control group (LPS + Oil), positive control group (LPS + DEX), LPS + VK2 (L) group (VK2, 1.5 mg/kg), and LPS + VK2 (H) group (VK2, 15 mg/kg). Hematoxylin–eosin (HE) staining of lung tissue was performed. Antioxidant superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) activities, and the Ca2+ level in the lung tissue were measured. The effects of VK2 on inflammation, apoptosis, tight junction (TJ) injury, mitochondrial dysfunction, and autophagy were quantitatively assessed using Western blot analysis. Compared with the LPS group, VK2 improved histopathological changes; alleviated inflammation, apoptosis, and TJ injury; increased antioxidant enzyme activity; reduced Ca2+ overload; regulated mitochondrial function; and inhibited lung autophagy. These results indicate that VK2 could improve tight junction protein loss, inflammation, and cell apoptosis in LPS-induced ALI by inhibiting the mitochondrial dysfunction and excessive autophagy, indicating that VK2 plays a beneficial role in ALI and might be a potential therapeutic strategy.

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“…C57BL/6 male mice were fed in an animal house with a constant temperature of 23 ± 2 °C, humidity of 60–75% and alternating light and dark per 12 h. Based on our previous studies 20 and preliminary experiments, we determined the dose of VK2 intervention in this experiment. After one week of adaptive feeding, a total of 42 mice were randomly divided into seven groups (n = 6): control group (C), control + vitamin K2 (0.1 mg/kg, 0.2 mg/kg and 0.4 mg/kg) group (C + VK2), high fat diet group (HFD), high fat diet + 0.1 mg/kg vitamin K2 group [HFD + VK2(L)], high fat diet + 0.2 mg/kg vitamin K2 group [HFD + VK2(M)], high fat diet + 0.4 mg/kg vitamin K2 [HFD + VK2(H)] group and high fat diet + vehicle group (HFD + V).…”

Section: Methodsmentioning

confidence: 99%

Vitamin K2 protects mice against non-alcoholic fatty liver disease induced by high-fat diet

Zhao,

Yang,

Xiao

et al. 2024

Sci Rep

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Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases worldwide and there is a huge unmet need to find safer and more effective drugs. Vitamin K has been found to regulate lipid metabolism in the liver. However, the effects of vitamin K2 on NAFLD is unclear. This study aims to evaluate the preventive and therapeutic effects of vitamin K2 in the process of fatty liver formation and to explore molecular mechanisms the associated with lipid metabolism. A non-alcoholic fatty liver model was established by high-fat diet administration for three months. Vitamin K2 significantly reduced the body weight, abdominal circumference and body fat percentage of NAFLD mice. Vitamin K2 also showed histological benefits in reducing hepatic steatosis. NAFLD mice induced by high-fat diet showed increased HMGR while vitamin K2 intervention could reverse the pathological lterations. Adiponectin (APN) is an endogenous bioactive polypeptide or protein secreted by adipocytes. We detected APN, SOD, AlaDH and other indicators that may affect the state of high-fat diet mice, but the experimental results showed that the above indicators did not change significantly. It is worth noting that the effect of vitamin K2 supplementation on the lipid-lowering effect of uc OC in vivo needs to be further explored. This study first reported the protective effect of vitamin K2 on high-fat diet-induced NAFLD in mice. The protective effect of vitamin K2 may be related to the improvement of lipid metabolism disorder in NAFLD.

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Vitamin K2 (MK-7) attenuates LPS-induced acute lung injury via inhibiting inflammation, apoptosis, and ferroptosis

Cited by 4 publications

References 64 publications

Vitamin K: a potential missing link in critical illness–a scoping review

Vitamin K: a potential missing link in critical illness–a scoping review

Protective Effect of Vitamin K2 (MK-7) on Acute Lung Injury Induced by Lipopolysaccharide in Mice

Vitamin K2 protects mice against non-alcoholic fatty liver disease induced by high-fat diet

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