Folate ameliorates homocysteine-induced osteoblast dysfunction by reducing endoplasmic reticulum stress-activated PERK/ATF-4/CHOP pathway in MC3T3-E1 cells

Su, Shan; Zhang, Di; Liu, Jinjin; Zhao, Hang; Tang, Xulei; Che, Hongxia; Wang, Qiangmei; Ren, Wanna; Zhen, Donghu

doi:10.1007/s00774-022-01313-x

Cited by 8 publications

(2 citation statements)

References 40 publications

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“…Similar beneficial effect of FA supplementation on bone density was observed in a model of cyclosporine-induced bone loss ( 295 ). Folic acid also ameliorated the adverse effect of homocysteine on osteoblast proliferation, differentiation and mineralization through inhibition of PERK-activated ERS ( 296 ). Folic acid potentiated osteoblastogenic effect of hydroxyapatite nanoparticles, as evidenced by a more profound RUNX2 expression in human mesenchymal stem cells ( 297 ).…”

Section: Group B Vitaminsmentioning

confidence: 99%

Role of vitamins beyond vitamin D₃ in bone health and osteoporosis (Review)

Skalny,

Aschner,

Tsatsakis

et al. 2023

Int J Mol Med

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The objective of the present review was to summarize the molecular mechanisms associated with the effects of the vitamins A, C, E and K, and group B vitamins on bone and their potential roles in the development of osteoporosis. Epidemiological findings have demonstrated an association between vitamin deficiency and a higher risk of developing osteoporosis; vitamins are positively related to bone health upon their intake at the physiological range. Excessive vitamin intake can also adversely affect bone formation, as clearly demonstrated for vitamin A. Vitamins E (tocopherols and tocotrienols), K 2 (menaquinones 4 and 7) and C have also been shown to promote osteoblast development through bone morphogenetic protein (BMP)/Smad and Wnt/β-catenin signaling, as well as the TGFβ/Smad pathway (α-tocopherol). Vitamin A metabolite (all-trans retinoic acid) exerts both inhibitory and stimulatory effects on BMP- and Wnt/β-catenin-mediated osteogenesis at the nanomolar and micromolar range, respectively. Certain vitamins significantly reduce receptor activator of nuclear factor kappa-B ligand (RANKL) production and RANKL/RANK signaling, while increasing the level of osteoprotegerin (OPG), thus reducing the RANKL/OPG ratio and exerting anti-osteoclastogenic effects. Ascorbic acid can both promote and inhibit RANKL signaling, being essential for osteoclastogenesis. Vitamin K 2 has also been shown to prevent vascular calcification by activating matrix Gla protein through its carboxylation. Therefore, the maintenance of a physiological intake of vitamins should be considered as a nutritional strategy for the prevention of osteoporosis.

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Section: Group B Vitaminsmentioning

confidence: 99%

Role of vitamins beyond vitamin D₃ in bone health and osteoporosis (Review)

Skalny,

Aschner,

Tsatsakis

et al. 2023

Int J Mol Med

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show abstract

“…In addition, p38 MAPK phosphorylation activates the transcription factor CHOP, which increases the expression of BIM and death receptor 5 (DR5) while decreasing that of BCL-2 to promote apoptosis [ 104 ]. Moreover, PERK overactivation can upregulate the CHOP/GADD153 transcription factor, which inhibits the antiapoptotic protein BCL-2 and enhances the expression of associated proapoptotic proteins [ 105 ]. A recent study has shown that the knockdown of CHOP and ATF4 by RNA interference can reduce the level of apoptosis in response to ER stress [ 106 ].…”

Section: Upr Signalingmentioning

confidence: 99%

Endoplasmic Reticulum Stress in Chronic Obstructive Pulmonary Disease: Mechanisms and Future Perspectives

Yang

et al. 2022

Biomolecules

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The endoplasmic reticulum (ER) is an integral organelle for maintaining protein homeostasis. Multiple factors can disrupt protein folding in the lumen of the ER, triggering ER stress and activating the unfolded protein response (UPR), which interrelates with various damage mechanisms, such as inflammation, apoptosis, and autophagy. Numerous studies have linked ER stress and UPR to the progression of chronic obstructive pulmonary disease (COPD). This review focuses on the mechanisms of other cellular processes triggered by UPR and summarizes drug intervention strategies targeting the UPR pathway in COPD to explore new therapeutic approaches and preventive measures for COPD.

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Advances in the interaction between endoplasmic reticulum stress and osteoporosis

Ming

Chen

et al. 2023

Biomedicine & Pharmacotherapy

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Folate ameliorates homocysteine-induced osteoblast dysfunction by reducing endoplasmic reticulum stress-activated PERK/ATF-4/CHOP pathway in MC3T3-E1 cells

Cited by 8 publications

References 40 publications

Role of vitamins beyond vitamin D₃ in bone health and osteoporosis (Review)

Role of vitamins beyond vitamin D₃ in bone health and osteoporosis (Review)

Endoplasmic Reticulum Stress in Chronic Obstructive Pulmonary Disease: Mechanisms and Future Perspectives

Advances in the interaction between endoplasmic reticulum stress and osteoporosis

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Folate ameliorates homocysteine-induced osteoblast dysfunction by reducing endoplasmic reticulum stress-activated PERK/ATF-4/CHOP pathway in MC3T3-E1 cells

Cited by 8 publications

References 40 publications

Role of vitamins beyond vitamin D3 in bone health and osteoporosis (Review)

Role of vitamins beyond vitamin D3 in bone health and osteoporosis (Review)

Endoplasmic Reticulum Stress in Chronic Obstructive Pulmonary Disease: Mechanisms and Future Perspectives

Advances in the interaction between endoplasmic reticulum stress and osteoporosis

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Resources

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Role of vitamins beyond vitamin D₃ in bone health and osteoporosis (Review)

Role of vitamins beyond vitamin D₃ in bone health and osteoporosis (Review)