Bone, inflammation and chronic kidney disease

Mazzaferro, Sandro; Martini, Natalia De; Rotondi, Silverio; Tartaglione, Lida; Ureña-Torres, Pablo; Bover, Jordi; Pasquali, Marzia

doi:10.1016/j.cca.2020.03.040

Cited by 29 publications

(28 citation statements)

References 42 publications

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“…An increased risk of fracture has been reported mainly in obese patients with type 2 diabetes mellitus, in whom the levels of the same cytokines are enhanced [ 90 ]. Similarly, a mineral bone disorder is evident in CKD, a pathology in which high levels of cytokines, including transforming growth factor-beta in addition to the others mentioned above, are correlated with the disease progression [ 91 ].…”

Section: Role Of Purine Enzymes In Bone Inflammatory Conditionsmentioning

confidence: 99%

In Search of a Role for Extracellular Purine Enzymes in Bone Function

et al. 2021

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Bone is one of the major tissues that undergoes continuous remodeling throughout life, thus ensuring both organic body growth during development and protection of internal organs as well as repair of trauma during adulthood. Many endogenous substances contribute to bone homeostasis, including purines. Their role has increasingly emerged in recent decades as compounds which, by interacting with specific receptors, can help determine adequate responses of bone cells to physiological or pathological stimuli. Equally, it is recognized that the activity of purines is closely dependent on their interconversion or metabolic degradation ensured by a series of enzymes present at extracellular level as predominantly bound to the cell membrane or, also, as soluble isoforms. While the effects of purines mediated by their receptor interactions have sufficiently, even though not entirely, been characterized in many tissues including bone, those promoted by the extracellular enzymes providing for purine metabolism have not been. In this review, we will try to circumstantiate the presence and the role of these enzymes in bone to define their close relationship with purine activities in maintaining bone homeostasis in normal or pathological conditions.

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Section: Role Of Purine Enzymes In Bone Inflammatory Conditionsmentioning

confidence: 99%

In Search of a Role for Extracellular Purine Enzymes in Bone Function

et al. 2021

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“…As bone mass decreases with aging, bone marrow fat increases (23) and secretes inhibitors of bone formation (such as tumor necrosis factorα and interleukin 6). In addition, systemic inflammation with aging, inflammaging (2,24,25) , results in increased mobilization of calcium from the bone (26) . This chronic negative calcium balance, when severe, diminishes bone strength and may lead to osteoporosis (26) .…”

Section: Introductionmentioning

confidence: 99%

“…In addition, systemic inflammation with aging, inflammaging, ( 2,24,25 ) results in increased mobilization of calcium from the bone. ( 26 ) This chronic negative calcium balance, when severe, diminishes bone strength and may lead to osteoporosis. ( 26 ) Osteoporosis predisposes to microcrack formation in the bone, which then further contributes to the inflammatory response.…”

Section: Introductionmentioning

confidence: 99%

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Renal Contributions to Age‐Related Changes in Mineral Metabolism

2021

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Aging results in a general decline in function in most systems. This is particularly true with respect to the skeleton and renal systems, impacting mineral homeostasis. Calcium and phosphate regulation requires tight coordination among the intestine, bone, parathyroid gland, and kidney.The role of the intestine is to absorb calcium and phosphate from the diet. The bone stores or releases calcium and phosphate depending on the body's needs. In response to low plasma ionized calcium concentration, the parathyroid gland produces parathyroid hormone which modulates bone turnover. The kidney reabsorbs or excretes the minerals and serves as the final regulator of plasma concentration. Many hormones are involved in this process in addition to parathyroid hormone, including fibroblast growth factor 23 produced by the bone, and calcitriol synthesized by the kidney. Sclerostin, calcitonin, osteoprotegerin and receptor activator of nuclear factor κ-B ligand also contribute to tissue-specific regulation. Changes in the function of organs due to aging or disease can perturb this balance. During aging, the intestine cannot absorb calcium efficiently due to decreased expression of key proteins. In the bone, the balance between bone formation and bone resorption tends toward the latter in older individuals. The kidney may not filter blood as efficiently in the later decades of life and the expression of certain proteins necessary for mineral homeostasis declines with age. These changes often lead to dysregulation of organismal mineral homeostasis. This review will focus on how mineral homeostasis is impacted by aging with a particular emphasis on the kidney's role in this process.

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“…Increased circulating inflammatory cytokines representing as chronic inflammatory condition among aged individuals contributes to development of osteoporosis, CVD and CKD.In patients with renal insufficiency, observed of bone and mineral disorders may accelerate aging and is a risk factor for cardiovascular death in these patients. Changes in mineral and bone metabolism in the early stages of CKD might accelerate aging, osteoporosis and CVD[75]. Thus association of common genes deregulated in CKD and SARS-CoV with arthritis and osteoporosis related disorders might represent relationship between CKD and these diseases.…”

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confidence: 99%

<strong>Molecular Basis of Kidney Defects in COVID-19 Patients</strong>

Pulai¹,

Basu²,

Saha³

et al. 2020

Preprint

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Background: Kidney damage is considered to be one of the risk factors for severity and mortality among COVID-19 patients. However, molecular nature of such observations remains unknown. Hypothesis: Altered gene expressions due to infection and in chronic kidney disease could explain severity in COVID-19 with kidney defects. Methods: We collected gene expression data from publicly available resources Gene Expression Omnibus CKD, Enrichr for deregulated genes in SARS-CoV infected cells in vitro, DisGeNET and others and carried out enrichment analysis using Enrichr. Result: Number of common genes altered in chronic kidney disease (CKD) and SARS-CoV infected cells was 2834. Enrichment analysis revealed that biological processes related viral life cycle and growth, cytokines, immunity, interferon, inflammation, apoptosis, autophagy, oxidative stress and others were significantly enriched with common deregulated genes. Similarly, significantly enriched pathways related to viral and bacterial infections, immunity and inflammation, cell cycle, ubiquitin mediated proteolysis, signaling pathways like Relaxin signaling pathway, mTOR signaling pathway, IL-17 signaling pathway, NF-kappa B signaling pathway were enriched with the common deregulated genes. These processes and pathways are known to be related to kidney damage. DisGeNET terms enriched include and related to Dengue fever, chronic Hepatitis, measles, retroviridae infections, respiratory syncytial virus Infections and many others. Kidney dysfunction related terms ischemia of kidney, renal fibrosis and diabetic nephropathy. Conclusion: Common deregulated genes in SARS-CoV infected cells and chronic kidney disease, as well as their enrichment with molecular processes and pathways relevant for viral pathogenesis and renal dysfunctions, could explain the severity of COVID-19 with kidney disease. This observation not only provides molecular relation of severity in COVID-19 with renal dysfunctions but might also help in the management and treatment targets for these cases.

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Bone, inflammation and chronic kidney disease

Cited by 29 publications

References 42 publications

In Search of a Role for Extracellular Purine Enzymes in Bone Function

In Search of a Role for Extracellular Purine Enzymes in Bone Function

Renal Contributions to Age‐Related Changes in Mineral Metabolism

<strong>Molecular Basis of Kidney Defects in COVID-19 Patients</strong>

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