Bone cell mechanosensitivity, estrogen deficiency, and osteoporosis

Klein‐Nulend, Jenneke; Oers, René F.M. van; Bakker, Astrid D.; Bacabac, Rommel G.

doi:10.1016/j.jbiomech.2014.12.007

Cited by 130 publications

(93 citation statements)

References 144 publications

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“…18 The cause of osteoporosis is multifactorial and includes genetic, hormonal and nutritional factors, combined with people's lifestyle choices. 19,20 Peak bone mass is reached early in adult life and from this point both men and women start to lose bone mass more or less depending on a combination of intrinsic and extrinsic factors. 21,22 This process can be aggravated by a lack of physical exercise, 23 prolonged treatment with corticoids, 24 estrogen deficiency, especially in postmenopausal women, 25 presence of other chronic diseases, and by aging.…”

Section: Introductionmentioning

confidence: 99%

“…21,22 This process can be aggravated by a lack of physical exercise, 23 prolonged treatment with corticoids, 24 estrogen deficiency, especially in postmenopausal women, 25 presence of other chronic diseases, and by aging. 20 Recent evidence has pointed out that autophagy, a cell survival pathway, plays an important role in the maintenance of bone homeostasis, [26][27][28] and changes in this pathway have been related to osteoporosis. 29,30 Since osteoporosis became a serious public health problem with an incidence rate that is likely to increase in the next decades, understanding the cellular and molecular mechanisms involved in the process of bone loss is crucial and paramount for the development of new therapies.…”

Section: Introductionmentioning

confidence: 99%

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Osteoporosis and autophagy: What is the relationship?

Florencio‐Silva

Sasso

Simões

et al. 2017

Rev. Assoc. Med. Bras.

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Autophagy is a survival pathway wherein non-functional proteins and organelles are degraded in lysosomes for recycling and energy production. Therefore, autophagy is fundamental for the maintenance of cell viability, acting as a quality control process that prevents the accumulation of unnecessary structures and oxidative stress. Increasing evidence has shown that autophagy dysfunction is related to several pathologies including neurodegenerative diseases and cancer. Moreover, recent studies have shown that autophagy plays an important role for the maintenance of bone homeostasis. For instance, in vitro and animal and human studies indicate that autophagy dysfunction in bone cells is associated with the onset of bone diseases such as osteoporosis. This review had the purpose of discussing the issue to confirm whether a relationship between autophagy dysfunction and osteoporosis exits.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Osteoporosis and autophagy: What is the relationship?

Florencio‐Silva

Sasso

Simões

et al. 2017

Rev. Assoc. Med. Bras.

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“…It is a key factor for PMOP that E2 deficiency strongly promotes bone resorption of osteoclasts 19, 20. However, the exactly cellular and molecular mechanisms of oestrogen deficiency‐increased osteoclastic bone resorption are not fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

Regulation of TRPV5 transcription and expression by E2/ERα signalling contributes to inhibition of osteoclastogenesis

Song

Lin

et al. 2018

J Cellular Molecular Medi

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The increasing of osteoclasts formation and activity because of oestrogen (E2) deficiency is very important in the aetiology of postmenopausal osteoporosis. Our previous studies showed that E2 inhibited osteoclastic bone resorption by increasing the expression of Transient Receptor Potential Vanilloid 5 (TRPV5) channel. However, the exact mechanism by which E2 increases TRPV5 expression is not fully elucidated. In this study, Western blot, quantitative real‐time PCR, tartrate‐resistant acid phosphatase staining, F‐actin ring staining, chromatin immunoprecipitation and luciferase assay were applied to explore the mechanisms that E2‐induced TRPV5 expression contributes to the inhibition of osteoclastogenesis. The results showed that silencing or overexpressing of TRPV5 significantly affected osteoclasts differentiation and activity. Silencing of TRPV5 obviously alleviated E2‐inhibited osteoclastogenesis, resulting in increasing of bone resorption. E2 stimulated mature osteoclasts apoptosis by increasing TRPV5 expression. Further studies showed that E2 increased TRPV5 expression through the interaction of the oestrogen receptor α (ERα) with NF‐κB, which could directly bind to the fragment of −286 nt ~ −277 nt in the promoter region of trpv5. Taken together, we conclude that TRPV5 plays a dominant effect in E2‐mediated osteoclasts formation, bone resorption activity and osteoclasts apoptosis. Furthermore, NF‐κB plays an important role in the transcriptional activation of E2‐ERα stimulated TRPV5 expression.

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“…LRP5-deficient mice were used and showed that the LRP5 mutation was associated with increased response to loading [76], while sclerostindeficient mice demonstrated that long-term sclerostin deficiency can result in increased bone formation [77]. Many studies using germ-line and targeted protein knockouts for estrogen and androgen pathways have investigated the role these pathways play in governing the response to mechanical loading [78][79][80][81]. A detailed discussion of these studies is beyond the scope of this paper but the reader is directed to a recent review on the topic [82].…”

Section: Page 8 Of 22mentioning

confidence: 99%

Bone Quality and Quantity are Mediated by Mechanical Stimuli

Berman

Wallace

2016

Clinic Rev Bone Miner Metab

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Prevention of fracture through improved bone mechanical strength is of great importance given the large number of bone disease-related fractures each year, the decreased quality of life associated with fractures, and the large anticipated increase in fracture incidence over the upcoming years due to the aging population. Exercise and other forms of mechanical stimulation have been shown to increase bone mass, suggesting improved strength. However, while bone mass is a good indicator of strength, other components (such as bone quality) also contribute to bone mechanical integrity. While increased bone mass has been explored considerably using both exercise and targeted loading models, the role of mechanical stimulation in altering bone quality has been explored to a lesser degree. Understanding how to improve both the quantity and quality of bone is critical to increasing fracture resistance. Herein, we discuss quantity and quality-based improvements that have been observed using both exercise and targeted loading models of bone adaptation.

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Bone cell mechanosensitivity, estrogen deficiency, and osteoporosis

Cited by 130 publications

References 144 publications

Osteoporosis and autophagy: What is the relationship?

Osteoporosis and autophagy: What is the relationship?

Regulation of TRPV5 transcription and expression by E2/ERα signalling contributes to inhibition of osteoclastogenesis

Bone Quality and Quantity are Mediated by Mechanical Stimuli

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