oxalate/inflammation

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Helper T-cell signaling and inflammatory pathway lead to formation of calcium phosphate but not calcium oxalate stones on Randall's plaques.

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To elucidate the difference in the lithogenesis of calcium oxalate and calcium phosphate stones.Renal papillary tissues were obtained from 23 idiopathic calcium oxalate and seven calcium phosphate stone patients who had undergone endoscopic lithotripsy.

H3 relaxin protects against calcium oxalate crystal-induced renal inflammatory pyroptosis

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Objectives: Calcium oxalate (CaOx) crystals can activate inflammatory cytokines by triggering inflammasomes, which cause damage to the adhered epithelium, a dysfunctional microenvironment and even renal failure. However, a comprehensive

The initial and subsequent inflammatory events during calcium oxalate lithiasis.

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BACKGROUND Crystallization is believed to be the initiation step of urolithiasis, even though it is unknown where inside the nephron the first crystal nucleation occurs. METHODS Direct nucleation of calcium oxalate and subsequent events including crystal retention, cellular damage, endocytosis, and

Evaluation of [(89)Zr]-Oxalate as a PET Tracer in Inflammation, Tumor, and Rheumatoid Arthritis Models.

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To obtain an additional pharmacological agent for the diagnosis of inflammation, we investigated the medical use of (89)Zr-oxalate as a positron emission tomography (PET) probe for the in vivo imaging of inflammation and compared its efficacy to that of 2-deoxy-2-[(18)F]fluoro-d-glucose ([(18)F]FDG)

Hydroxycitric acid inhibits renal calcium oxalate deposition by reducing oxidative stress and inflammation.

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To evaluate the preventive effects of hydroxycitric acid（HCA） for stone formation in the glyoxylate-induced mouse model.Male C57BL/6J mice were divided into a control group, a glyoxylate(GOX) 100 mg/kg group, a GOX+HCA 100 mg/kg group, and a GOX+HCA 200

Transcriptional study of hyperoxaluria and calcium oxalate nephrolithiasis in male rats: Inflammatory changes are mainly associated with crystal deposition.

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Hyperoxaluria associated with renal deposition of calcium oxalate (CaOx) crystals causes renal injury and inflammation leading to number of diseases including chronic kidney disease (CKD). It is however, not been possible to separate the renal consequences of hyperoxaluria from that of CaOx crystal

Reactive oxygen species, inflammation and calcium oxalate nephrolithiasis.

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Calcium oxalate (CaOx) kidney stones are formed attached to Randall's plaques (RPs) or Randall's plugs. Mechanisms involved in the formation and growth are poorly understood. It is our hypothesis that stone formation is a form of pathological biomineralization or ectopic calcification. Pathological

Inhibiting inflammation and modulating oxidative stress in oxalate-induced nephrolithiasis with the Nrf2 activator dimethyl fumarate.

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Hyperoxaluria induces oxidative stress, and inflammation causes renal epithelial cell injury in nephrolithiasis, suggesting that reduced oxalate toxicity may be beneficial. This study aimed to investigate whether nuclear factor (erythroid-derived 2)-like 2 (Nrf2, also called Nfe2l2) induced by

Sulforaphane elicts dual therapeutic effects on Renal Inflammatory Injury and crystal deposition in Calcium Oxalate Nephrocalcinosis

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Intrarenal calcium oxalate (CaOx) crystals induce renal tubular epithelial cells (TECs) injury and inflammation, which involve Toll-like receptor 4 (TLR4)/interferon regulatory factor 1 (IRF1) signaling. Additionally, infiltrating macrophages (Mϕs) might influence intrarenal CaOx crystals and

Calcium Oxalate Differentiates Human Monocytes Into Inflammatory M1 Macrophages.

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UNASSIGNED A number of hyperoxaluric states have been associated with calcium oxalate (CaOx) deposits in the kidneys. In animal models of stone disease, these crystals interact with circulating monocytes that have migrated into the kidney as part of innate immunity. Similarly, macrophages surround

NALP3-mediated inflammation is a principal cause of progressive renal failure in oxalate nephropathy.

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Oxalate nephropathy with renal failure is caused by multiple disorders leading to hyperoxaluria due to either overproduction of oxalate (primary hyperoxaluria) or excessive absorption of dietary oxalate (enteric hyperoxaluria). To study the etiology of renal failure in crystal-induced kidney

[The role of cell-crystal reaction mediated inflammation in the formation of intrarenal calcium oxalate crystals].

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Calcium oxalate nephrolithiasis is the common disease of urinary surgery, its exact pathogenesis is still unclear.It is believed that the renal inflammatory injury induced by cell-crystal reaction plays an important role in the formation of intrarenal calcium oxalate crystals. Recent studies

Atorvastatin inhibits renal inflammatory response induced by calcium oxalate crystals via inhibiting the activation of TLR4/NF-κB and NLRP3 inflammasome.

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This study aimed to investigate the renal protective effect of atorvastatin (ATV) on the kidney inflammation induced by calcium oxalate (CaOx) crystals. A cell model of cell-crystal interactions and a rat model of CaOx kidney stone were established. The expressions of TLR4, NF-κB, NLRP3, and cleaved

LncRNA HOXA11-AS regulates calcium oxalate crystal-induced renal inflammation via miR-124-3p/MCP-1.

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Long noncoding RNA (lncRNA) has been suggested to play an important role in a variety of diseases over the past decade. In a previous study, we identified a novel lncRNA, termed HOXA11-AS, which was significantly up-regulated in calcium oxalate (CaOx) nephrolithiasis. However, the biological

Calcium oxalate crystals induce renal inflammation by NLRP3-mediated IL-1β secretion.

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Nephrocalcinosis, acute calcium oxalate (CaOx) nephropathy, and renal stone disease can lead to inflammation and subsequent renal failure, but the underlying pathological mechanisms remain elusive. Other crystallopathies, such as gout, atherosclerosis, and asbestosis, trigger inflammation and tissue

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