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1

Halverson, Paul B., and Beth A. Derfus. "Calcium crystal–induced inflammation." Current Opinion in Rheumatology 13, no. 3 (2001): 221–24. http://dx.doi.org/10.1097/00002281-200105000-00013.

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2

Landis, R. Clive, and Dorian O. Haskard. "Pathogenesis of crystal-induced inflammation." Current Rheumatology Reports 3, no. 1 (2001): 36–41. http://dx.doi.org/10.1007/s11926-001-0049-7.

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3

Lan, Zhou, Lvyi Chen, Jing Feng, et al. "Mechanosensitive TRPV4 is required for crystal-induced inflammation." Annals of the Rheumatic Diseases 80, no. 12 (2021): 1604–14. http://dx.doi.org/10.1136/annrheumdis-2021-220295.

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Crystal structures activate innate immune cells, especially macrophages and initiate inflammatory responses. We aimed to understand the role of the mechanosensitive TRPV4 channel in crystal-induced inflammation. Real-time RT-PCR, RNAscope in situ hybridisation, and Trpv4eGFP mice were used to examine TRPV4 expression and whole-cell patch-clamp recording and live-cell Ca2+ imaging were used to study TRPV4 function in mouse synovial macrophages and human peripheral blood mononuclear cells (PBMCs). Both genetic deletion and pharmacological inhibition approaches were used to investigate the role o
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4

Terkeltaub, Robert A. "Gout and mechanisms of crystal-induced inflammation." Current Opinion in Rheumatology 5, no. 4 (1993): 510–16. http://dx.doi.org/10.1097/00002281-199305040-00017.

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5

Getting, Stephen J., Connie W. Lam, Airu S. Chen, Paolo Grieco, and Mauro Perretti. "Melanocortin 3 receptors control crystal‐induced inflammation." FASEB Journal 20, no. 13 (2006): 2234–41. http://dx.doi.org/10.1096/fj.06-6339com.

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6

Akahoshi, Tohru, Yousuke Murakami, and Hidero Kitasato. "Recent advances in crystal-induced acute inflammation." Current Opinion in Rheumatology 19, no. 2 (2007): 146–50. http://dx.doi.org/10.1097/bor.0b013e328014529a.

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7

Pham, N., T. W. Chirayath, F. Castelli, et al. "POS0510 INTERMITTENT FASTING REDUCES CRYSTAL-INDUCED INFLAMMATION." Annals of the Rheumatic Diseases 82, Suppl 1 (2023): 517. http://dx.doi.org/10.1136/annrheumdis-2023-eular.5106.

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BackgroundInflammation induced by monosodium urate (MSU) and calcium pyrophosphate (CPP) crystals depends on interleukin (IL)-1β activated by the NLRP3 inflammasome. The inflammatory response can be modulated by diet, fasting, and caloric restriction.ObjectivesTo determine whether intermittent fasting reduces MSU and CPP crystal-induced inflammation.MethodsCrystal-induced inflammation was assessed using both types of crystalsin vivoin the air pouch model in 8-week-old wild-type male mice fed either with a normal ad libitum diet or intermittent fasting (IF) (every over day fast, 2 days during 1
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8

Tsay, Gregory, Jia-Hau Yen, Ling Chung Lin, Pui Ying Leong, Jiunn-Horng Chen та Zsuzsa Szondy. "The MTA1-TG2 is involved in self-limitation of monosodium urate crystal-induced inflammation by upregulating the levels of active TGFβ1 leading to inhibition of JAK2 signaling (HUM1P.305)". Journal of Immunology 194, № 1_Supplement (2015): 52.30. http://dx.doi.org/10.4049/jimmunol.194.supp.52.30.

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Abstract Abstract Introduction: Transglutaminase 2 (TG2), a protein crosslinking enzyme with multiple biochemical functions, has been connected to various inflammatory processes. In this study, the involvement of TG2 in monosodium urate (MSU) crystal-induced inflammation was studied. Conclusions: These findings reveal an inherent regulatory role of the MTA1-TG2 pathway in the self-limitation of MSU crystal-induced inflammation via positively regulating the levels of active TGF-b in macrophages that opposes the MSU crystal- induced JAK2 -dependent pro-inflammatory cytokine formation.
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Rasool, Mahaboobkhan, Sonal Chandal, and Evan Prince Sabina. "Inhibition of Monosodium Urate Crystal-Induced Inflammation by Withaferin A." Journal of Pharmacy & Pharmaceutical Sciences 11, no. 4 (2009): 46. http://dx.doi.org/10.18433/j35k58.

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ABSTRACT 
 Purpose. Gouty arthritis is a characteristically intense acute inflammatory reaction resulting from the formation of sodium urate crystals in the joint cavity. In the present study, the effect of withaferin A, a steroidal lactone was investigated on monosodium urate crystal-induced inflammation in mice; an experimental model for gouty arthritis and compared it with that of the non-steroidal anti-inflammatory drug, indomethacin. 
 Methods. Paw volume and levels/activities of lysosomal enzymes, lipid peroxidation, anti-oxidant status and inflammatory mediator TNF-α were dete
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10

Galozzi, Paola, Lucia Maschio, Samuela Carraro, Anna Scanu, Monica Facco, and Francesca Oliviero. "M2 macrophages as resolvers of crystal-induced inflammation." Rheumatology 60, no. 5 (2021): 2480–83. http://dx.doi.org/10.1093/rheumatology/keab122.

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11

Woolf, A. D., and P. A. Dieppe. "Mediators of crystal-induced inflammation in the joint." British Medical Bulletin 43, no. 2 (1987): 429–44. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072192.

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12

Weinberger, Abraham. "Gout, uric acid metabolism, and crystal-induced inflammation." Current Opinion in Rheumatology 7, no. 4 (1995): 359–63. http://dx.doi.org/10.1097/00002281-199507000-00017.

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13

Jiang, Hui, Feng Chen, DianZe Song, Xiaoqin Zhou, Long Ren, and Mei Zeng. "Dynamin-Related Protein 1 Is Involved in Mitochondrial Damage, Defective Mitophagy, and NLRP3 Inflammasome Activation Induced by MSU Crystals." Oxidative Medicine and Cellular Longevity 2022 (October 25, 2022): 1–22. http://dx.doi.org/10.1155/2022/5064494.

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Excessive generation of reactive oxygen species (ROS) has great impacts on MSU crystal-induced inflammation. Drp1-dependent mitochondrial fission is closely associated with mitochondrial ROS levels. However, whether Drp1 signaling contributes to MSU crystal-induced inflammation remains unclear. Mice bone marrow-derived macrophages (BMDMs) were primed with LPS and then stimulated with MSU suspensions for 12 h. The protein levels associated with mitochondrial dynamics, oxidative stress, and mitophagy were detected by Western blot. BMDMs were loaded with MitoTracker Green probe to detect mitochon
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14

Meiliana, Anna, and Andi Wijaya. "Inflammation and Atherosclerosis: Current Pathogenesis." Indonesian Biomedical Journal 4, no. 2 (2012): 73. http://dx.doi.org/10.18585/inabj.v4i2.165.

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BACKGROUND: The inflammatory nature of atherosclerosis is well established but the agent(s) that incite inflammation in the artery wall remain largely unknown.CONTENT: Chronic inflammation is recognized as a major driving force in atherogenesis. The sites of atherosclerotic plaque development in the arterial wall are characterized by cholesterol accumulation and infiltration of peripheral blood monocytes, which gradually differentiate into macrophages. Cholesterol crystals, the common constituents of atherosclerotic lesions, include NLRP3 inflammasome activation and IL-1β secretion in human ma
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15

Ray, Katrina. "NLRP3 inflammasome mediates crystal-induced joint inflammation and dysfunction." Nature Reviews Rheumatology 7, no. 12 (2011): 684. http://dx.doi.org/10.1038/nrrheum.2011.164.

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16

Brooks, P. M., D. Burton, and M. J. Forrest. "Crystal-induced inflammation in the rat subcutaneous air-pouch." British Journal of Pharmacology 90, no. 2 (1987): 413–19. http://dx.doi.org/10.1111/j.1476-5381.1987.tb08971.x.

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17

TERASAWA, Michio, Hidekazu ARATANI, Yoshinori IWAHISA, Tomonori IMAYOSHI, and Yutaka MARUYAMA. "Effect of pranoprofen on sodium urate crystal-induced inflammation." Folia Pharmacologica Japonica 89, no. 3 (1987): 129–37. http://dx.doi.org/10.1254/fpj.89.129.

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18

MAEDA, Etsuko, Toshio HUJIYOSHI, and Toshio UEMATSU. "Effects of alminoprofen on sodium urate crystal-induced inflammation." Folia Pharmacologica Japonica 98, no. 6 (1991): 467–74. http://dx.doi.org/10.1254/fpj.98.6_467.

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19

Lioté, Frédéric, and Hang-Korng Ea. "Recent developments in crystal-induced inflammation pathogenesis and management." Current Rheumatology Reports 9, no. 3 (2007): 243–50. http://dx.doi.org/10.1007/s11926-007-0039-5.

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20

Klinkhammer, Barbara Mara, Sonja Djudjaj, Uta Kunter, et al. "Cellular and Molecular Mechanisms of Kidney Injury in 2,8-Dihydroxyadenine Nephropathy." Journal of the American Society of Nephrology 31, no. 4 (2020): 799–816. http://dx.doi.org/10.1681/asn.2019080827.

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BackgroundHereditary deficiency of adenine phosphoribosyltransferase causes 2,8-dihydroxyadenine (2,8-DHA) nephropathy, a rare condition characterized by formation of 2,8-DHA crystals within renal tubules. Clinical relevance of rodent models of 2,8-DHA crystal nephropathy induced by excessive adenine intake is unknown.MethodsUsing animal models and patient kidney biopsies, we assessed the pathogenic sequelae of 2,8-DHA crystal-induced kidney damage. We also used knockout mice to investigate the role of TNF receptors 1 and 2 (TNFR1 and TNFR2), CD44, or alpha2-HS glycoprotein (AHSG), all of whic
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21

Chung, Yeon-Ho, Doo Hyun Chung та Won-Woo Lee. "Inhibition of phosphorylation of 4E-BP1 by resveratrol suppresses monosodium urate crystal-induced production of interleukin-1β in human monocytes (IRM5P.646)". Journal of Immunology 194, № 1_Supplement (2015): 59.11. http://dx.doi.org/10.4049/jimmunol.194.supp.59.11.

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Abstract Monosodium urate (MSU) crystal-induced production of interleukin-1β(IL-1β) from innate immune cells has a critical role for the pathogenesis of gouty inflammation. Recently, it has been reported that resveratrol has a protective effect on gouty arthritis in mouse model. However, the underlying mechanism remains unknown. In this study, we investigated the immunoregulatory role of resveratrol affecting MSU crystal-induced IL-1β production in human CD14+ monocytes. Our data showed that resveratrol inhibited the release of IL-1β by monocyte in response to MSU crystal stimulation and it wa
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22

Liu, Lei, Chen Lin, Xiu Li, et al. "Protective Effect of Alkaline Mineral Water on Calcium Oxalate-Induced Kidney Injury in Mice." Evidence-Based Complementary and Alternative Medicine 2023 (October 25, 2023): 1–10. http://dx.doi.org/10.1155/2023/4559802.

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Background. Kidney stone disease induces chronic renal insufficiency by crystal-induced renal tubular epithelial cell injury. It has been reported that the prevalence of kidney stone disease is increasing, accompanied by the high recurrence rate. Alkaline mineral water has been reported to possess beneficial effects to attenuate inflammation. Here, we explored the potential protective effects and underlying mechanisms of alkaline mineral water against calcium oxalate-induced kidney injury. Methods. We performed the mice kidney stone model by administering glyoxylate at 100 mg/kg once daily for
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23

Sellmayr, Markus, Moritz Roman Hernandez Petzsche, Qiuyue Ma, et al. "Only Hyperuricemia with Crystalluria, but not Asymptomatic Hyperuricemia, Drives Progression of Chronic Kidney Disease." Journal of the American Society of Nephrology 31, no. 12 (2020): 2773–92. http://dx.doi.org/10.1681/asn.2020040523.

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BackgroundThe roles of asymptomatic hyperuricemia or uric acid (UA) crystals in CKD progression are unknown. Hypotheses to explain links between UA deposition and progression of CKD include that (1) asymptomatic hyperuricemia does not promote CKD progression unless UA crystallizes in the kidney; (2) UA crystal granulomas may form due to pre-existing CKD; and (3) proinflammatory granuloma-related M1-like macrophages may drive UA crystal-induced CKD progression.MethodsMALDI-FTICR mass spectrometry, immunohistochemistry, 3D confocal microscopy, and flow cytometry were used to characterize a novel
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24

Galozzi, Paola, Sara Bindoli, Roberto Luisetto, et al. "Regulation of crystal induced inflammation: current understandings and clinical implications." Expert Review of Clinical Immunology 17, no. 7 (2021): 773–87. http://dx.doi.org/10.1080/1744666x.2021.1937129.

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25

Janoudi, Abed, Fadi E. Shamoun, Jagadeesh K. Kalavakunta, and George S. Abela. "Cholesterol crystal induced arterial inflammation and destabilization of atherosclerotic plaque." European Heart Journal 37, no. 25 (2015): 1959–67. http://dx.doi.org/10.1093/eurheartj/ehv653.

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26

Scanu, Anna, Roberto Luisetto, Francesca Oliviero, et al. "High-density lipoproteins inhibit urate crystal-induced inflammation in mice." Annals of the Rheumatic Diseases 74, no. 3 (2013): 587–94. http://dx.doi.org/10.1136/annrheumdis-2013-203803.

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27

Inokuchi, Taku, Tuneyoshi Ka, Asako Yamamoto, et al. "RETRACTED: Effects of ethanol on monosodium urate crystal-induced inflammation." Cytokine 42, no. 2 (2008): 198–204. http://dx.doi.org/10.1016/j.cyto.2008.01.001.

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28

Bakke, Siril S., Marie H. Aune, Nathalie Niyonzima, et al. "Cyclodextrin Reduces Cholesterol Crystal–Induced Inflammation by Modulating Complement Activation." Journal of Immunology 199, no. 8 (2017): 2910–20. http://dx.doi.org/10.4049/jimmunol.1700302.

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29

Klaassen-Broekema, N., and O. P. van Bijsterveld. "The red eye of renal failure: a crystal induced inflammation?" British Journal of Ophthalmology 76, no. 10 (1992): 578–81. http://dx.doi.org/10.1136/bjo.76.10.578.

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30

Inokuchi, Taku, Tuneyoshi Ka, Asako Yamamoto, et al. "RETRACTED: Effects of ethanol on monosodium urate crystal-induced inflammation." Cytokine 110 (October 2018): 484. http://dx.doi.org/10.1016/j.cyto.2018.03.014.

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31

Orellano, Laura, Kennet Rock, and Jiann-Jyh Lai. "Therapeutic potential of VBY-825 in MSU crystal-induced NLRP3 inflammasome activation." Journal of Immunology 212, no. 1_Supplement (2024): 0957_5533. http://dx.doi.org/10.4049/jimmunol.212.supp.0957.5533.

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Abstract In gout patients, MSU crystals formed in the joints cause inflammation, and the activation of the NLRP3 inflammasome is believed to mediate these responses. Cathepsins play an important role in crystal-induced NLRP3 activation that results in subsequent speck formation, caspase-1 activation, IL-1β secretion, and pyroptosis. In this study, we investigated if cathepsins can also influence MSU-induced NLRP3 activation in a gout mouse model. VBY-825 is a reversible pan-cathepsin inhibitor, and we found that VBY-825 significantly suppressed IL-1β secretion and LDH levels from peritoneal na
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32

Chirayath, T. W., N. Pham, C. Duranton, et al. "POS1169 THE INFLAMMATION INDUCED BY MONOSODIUM URATE AND CALCIUM PYROPHOSPHATE CRYSTALS DEPENDS ON OSMOLARITY AND AQUAPORIN CHANNELS." Annals of the Rheumatic Diseases 81, Suppl 1 (2022): 913.1–913. http://dx.doi.org/10.1136/annrheumdis-2022-eular.3571.

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BackgroundThe inflammation induced by monosodium urate (MSU) and calcium pyrophosphate (CPP) crystals is driven by interleukin (IL)-1β production. This later relies on NLRP3 inflammasome which can be activated by variation of ion concentration.ObjectivesTo assess the role of osmolarity and water flux in MSU and CPP crystal-induced inflammation.MethodsIn vitro, THP1 monocytes were stimulated by pyrogen-free synthetic MSU and CPP crystals in iso-, hypo- or hyperosmotic media. Cytokine production was quantified by ELISA in cell culture supernatants. Cell size was measured using video microscopy.
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Goo, Bonhyuk, Jeeyoun Lee, Chansol Park, Taeyoung Yune, and Yeoncheol Park. "Bee Venom Alleviated Edema and Pain in Monosodium Urate Crystals-Induced Gouty Arthritis in Rat by Inhibiting Inflammation." Toxins 13, no. 9 (2021): 661. http://dx.doi.org/10.3390/toxins13090661.

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Bee venom (BV) acupuncture has anti-inflammatory and analgesic effects; therefore, it was used as a traditional Korean medicine for various musculoskeletal disorders, especially arthritis. In this study, we investigated the effect of BV on monosodium urate (MSU) crystal-induced acute gouty rats. An intra-articular injection of MSU crystal suspension (1.25 mg/site) was administered to the tibiotarsal joint of the hind paw of Sprague Dawley rats to induce MSU crystal-induced gouty arthritis. Colchicine (30 mg/kg) was orally administered 1 h before MSU crystal injection as a positive control, and
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34

Oliviero, F., A. Scanu, R. Luisetto, et al. "THU0527 Epigallocatechin Gallate Suppresses Monosodium Urate Crystal-Induced Inflammation in Mice." Annals of the Rheumatic Diseases 73, Suppl 2 (2014): 365.2–365. http://dx.doi.org/10.1136/annrheumdis-2014-eular.4306.

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35

Oliviero, F., A. Scanu, G. Ceolotto, P. Sfriso, P. Spinella, and L. Punzi. "FRI0036 Epigallocatechin gallate modulates SIRT1 expression in CPP crystal-induced inflammation." Annals of the Rheumatic Diseases 71, Suppl 3 (2013): 321.3–322. http://dx.doi.org/10.1136/annrheumdis-2012-eular.2493.

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36

Raucci, Federica, Asif J. Iqbal, Anella Saviano, et al. "IL-17A neutralizing antibody regulates monosodium urate crystal-induced gouty inflammation." Pharmacological Research 147 (September 2019): 104351. http://dx.doi.org/10.1016/j.phrs.2019.104351.

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37

Nuki, George. "Colchicine: Its mechanism of action and efficacy in crystal-induced inflammation." Current Rheumatology Reports 10, no. 3 (2008): 218–27. http://dx.doi.org/10.1007/s11926-008-0036-3.

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38

Malawista, Stephen E., Gordon W. Duff, Elisha Atkins, Herman S. Cheung, and Daniel J. McCarty. "Crystal-induced endogenous pyrogen production. A further look at gouty inflammation." Arthritis & Rheumatism 28, no. 9 (1985): 1039–46. http://dx.doi.org/10.1002/art.1780280911.

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39

Sugino, Teruaki, Atsushi Okada, Kazumi Taguchi та ін. "Brown adipocytes and β3-stimulant-induced brown-like adipocytes contribute to the prevention of renal crystal formation". American Journal of Physiology-Renal Physiology 316, № 6 (2019): F1282—F1292. http://dx.doi.org/10.1152/ajprenal.00523.2018.

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According to recent studies, kidney stones are associated with metabolic syndrome. We focused on brown adipocytes and β3-stimulant-induced brown-like adipocytes to investigate how these adipocytes influence kidney stone disease. For the interscapular brown adipose tissue (iBAT) removal experiment, mice were subjected to either iBAT removal or sham operation (X-BAT group or sham group), and, after 3 wk, renal crystal deposition was induced by intra-abdominal injection of glyoxylate (GOX) for 6 days. For the β3-stimulant experiment, mice were administered intra-abdominal injections of the β3-sti
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Sil, Payel, Craig Hayes, Barbara Reaves, Jeremy Sokolove, and Balazs Rada. "NET formation induced by gout-associated monosodium urate crystals requires IL-8-mediated neutrophil migration and is inhibited by the P2Y6 receptor antagonist MRS2578." Journal of Immunology 196, no. 1_Supplement (2016): 119.6. http://dx.doi.org/10.4049/jimmunol.196.supp.119.6.

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Abstract Human neutrophils generate inflammatory responses within the joints of gout patients upon encountering Monosodium Urate (MSU) crystals. Studies (including ours) show that neutrophil extracellular traps (NETs) are found abundantly in the synovial fluid (SF) of gout patients and are crucial for the onset of the autoinflammatory cascade. Our goal is to shed light on possible roles of purinergic signaling and neutrophil migration in mediating in vitro NET formation induced by MSU crystals. Our data show that gout SF supernatants have significantly higher levels of the neutrophil granule m
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Taguchi, Kazumi, Atsushi Okada, Shuzo Hamamoto та ін. "Differential Roles of Peroxisome Proliferator-Activated Receptor-αand Receptor-γon Renal Crystal Formation in Hyperoxaluric Rodents". PPAR Research 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/9605890.

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Peroxisome proliferator-activated receptors (PPARs) and related inflammatory and oxidative molecule expression were investigated in a hyperoxaluric rodent model to evaluate thein vivoefficacy of PPAR agonists in preventing renal crystal formation. PPAR expression was examined in a mouse hyperoxaluria kidney stone model induced by daily intra-abdominal glyoxylate injection. Therapeutic effects of the PPARαagonist fenofibrate and PPARγagonist pioglitazone were also assessed in a 1% ethylene glycol-induced rat model of hyperoxaluria. Crystal formation, inflammation, cell injury, apoptosis, and ox
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42

Kim, Tehyung, Sueli de Oliveira Silva Lautenschlager, Qiuyue Ma, et al. "Drug Crystal-Related Gastrointestinal Complications Involve Crystal-Induced Release of Neutrophil and Monocyte Extracellular Traps." Cells 9, no. 11 (2020): 2481. http://dx.doi.org/10.3390/cells9112481.

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Ion-exchange resins are commonly used to manage complications of chronic kidney disease, such as hyperphosphatemia, hyperkalemia, and hypercholesterolemia. Occasionally, these drugs can irritate the gastrointestinal lining and cause life-threatening intestinal necrosis. Currently, the pathophysiology of drug crystal-induced intestinal necrosis is not well understood. We hypothesized that crystals of ion-exchange resins like sevelamer, polystyrene sulfonate, and cholestyramine can trigger the formation of neutrophil and monocyte extracellular traps by contributing to intestinal barrier dysfunct
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Liu, Xiao, Peng Yuan, Xifeng Sun, and Zhiqiang Chen. "Hydroxycitric Acid Inhibits Renal Calcium Oxalate Deposition by Reducing Oxidative Stress and Inflammation." Current Molecular Medicine 20, no. 7 (2020): 527–35. http://dx.doi.org/10.2174/1566524020666200103141116.

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Objective: The study aimed to evaluate the preventive effects of hydroxycitric acid(HCA) for stone formation in the glyoxylate-induced mouse model. Materials and methods: Male C57BL/6J mice were divided into a control group, glyoxylate(GOX) 100 mg/kg group, a GOX+HCA 100 mg/kg group, and a GOX+HCA 200 mg/kg group. Blood samples and kidney samples were collected on the eighth day of the experiment. We used Pizzolato staining and a polarized light microscope to examine crystal formation and evaluated oxidative stress via the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutat
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Renaudin, Felix, Lucie Orliaguet, Florence Castelli та ін. "Gout and pseudo-gout-related crystals promote GLUT1-mediated glycolysis that governs NLRP3 and interleukin-1β activation on macrophages". Annals of the Rheumatic Diseases 79, № 11 (2020): 1506–14. http://dx.doi.org/10.1136/annrheumdis-2020-217342.

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ObjectiveMacrophage activation by monosodium urate (MSU) and calcium pyrophosphate (CPP) crystals mediates an interleukin (IL)-1β-dependent inflammation during gout and pseudo-gout flare, respectively. Since metabolic reprogramming of macrophages goes along with inflammatory responses dependently on stimuli and tissue environment, we aimed to decipher the role of glycolysis and oxidative phosphorylation in the IL-1β-induced microcrystal response.MethodsBriefly, an in vitro study (metabolomics and real-time extracellular flux analysis) on MSU and CPP crystal-stimulated macrophages was performed
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45

Pouliot, Marc, Michael J. James, Shaun R. McColl, Paul H. Naccache, and Leslie G. Cleland. "Monosodium Urate Microcrystals Induce Cyclooxygenase-2 in Human Monocytes." Blood 91, no. 5 (1998): 1769–76. http://dx.doi.org/10.1182/blood.v91.5.1769.

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Abstract The formation and deposition of monosodium urate (MSU) microcrystals in articular and periarticular tissues is the causative agent of acute or chronic inflammatory responses known as gouty arthritis. Mononuclear phagocyte activation is involved in early triggering events of gout attacks. Because stimulated mononuclear phagocytes can constitute an important source of the inducible isoform of cyclooxygenase (COX-2), we evaluated the effects that proinflammatory microcrystals might have on COX-2 protein expression in crystal-stimulated monocytes. We found that MSU crystals, but not calci
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46

Pouliot, Marc, Michael J. James, Shaun R. McColl, Paul H. Naccache, and Leslie G. Cleland. "Monosodium Urate Microcrystals Induce Cyclooxygenase-2 in Human Monocytes." Blood 91, no. 5 (1998): 1769–76. http://dx.doi.org/10.1182/blood.v91.5.1769.1769_1769_1776.

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The formation and deposition of monosodium urate (MSU) microcrystals in articular and periarticular tissues is the causative agent of acute or chronic inflammatory responses known as gouty arthritis. Mononuclear phagocyte activation is involved in early triggering events of gout attacks. Because stimulated mononuclear phagocytes can constitute an important source of the inducible isoform of cyclooxygenase (COX-2), we evaluated the effects that proinflammatory microcrystals might have on COX-2 protein expression in crystal-stimulated monocytes. We found that MSU crystals, but not calcium pyroph
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Huang, Jingqun, Miaozhang Zhu, Ye Tao, et al. "Therapeutic properties of quercetin on monosodium urate crystal-induced inflammation in rat." Journal of Pharmacy and Pharmacology 64, no. 8 (2012): 1119–27. http://dx.doi.org/10.1111/j.2042-7158.2012.01504.x.

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Oliviero, F., A. Scanu, P. Galozzi, et al. "AB0063 Resveratrol Suppresses Crystal-Induced Inflammation in Vitro by Inhibiting Cytokine Production." Annals of the Rheumatic Diseases 74, Suppl 2 (2015): 911.3–911. http://dx.doi.org/10.1136/annrheumdis-2015-eular.5753.

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Nidorf, Stefan M., John W. Eikelboom, and Peter L. Thompson. "Targeting Cholesterol Crystal-Induced Inflammation for the Secondary Prevention of Cardiovascular Disease." Journal of Cardiovascular Pharmacology and Therapeutics 19, no. 1 (2013): 45–52. http://dx.doi.org/10.1177/1074248413499972.

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Yao, Xiujuan, Zuoqi Ding, Yufeng Xia, et al. "Inhibition of monosodium urate crystal-induced inflammation by scopoletin and underlying mechanisms." International Immunopharmacology 14, no. 4 (2012): 454–62. http://dx.doi.org/10.1016/j.intimp.2012.07.024.

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