The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.
Activation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1β in type 2 diabetes
Open accessAbstract
Interleukin 1β (IL-1β) is an important inflammatory mediator of type 2 diabetes. Here we show that oligomers of islet amyloid polypeptide (IAPP), a protein that forms amyloid deposits in the pancreas during type 2 diabetes, triggered the NLRP3 inflammasome and generated mature IL-1β. One therapy for type 2 diabetes, glyburide, suppressed IAPP-mediated IL-1β production in vitro. Processing of IL-1β initiated by IAPP first required priming, a process that involved glucose metabolism and was facilitated by minimally oxidized low-density lipoprotein. Finally, mice transgenic for human IAPP had more IL-1β in pancreatic islets, which localized together with amyloid and macrophages. Our findings identify previously unknown mechanisms in the pathogenesis of type 2 diabetes and treatment of pathology caused by IAPP.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“that induce interleukin (IL)-1β release to recruit macrophages and enhance local islet inflammation ( 45 ).”
From β-Cell Failure in Type 2 Diabetes: Postulated Mechanisms and Prospects for Prevention and Treatment (2014) · cites this paper as [45]
Experimental — accuracy not yet measuredIn the citing paper
“A potential role for NLRP3 in promoting elevated levels of IL-1β in type 2 diabetes was also implied by the observation of NLRP3-dependent IL-1β secretion by mouse bone marrow-derived macrophages and dendritic cells in response to islet amyloid polypeptide (IAPP), which is deposited in the pancreas and associated with loss of β-cell function in type 2 diabetes61.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [61]
In the citing paper
“Interestingly, the anti-diabetic drug glyburide (Glibenclamide; Roche/Sanofi-Aventis) has been shown to block glucose-mediated secretion of IL-1β by mouse pancreatic islets62, as well as IL-1β production by macrophages in response to IAPP61, and NLRP3-deficient mice were more glucose tolerant than wild-type mice62.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [61]
In the citing paper
“In a separate study, no differences in IL-1β secretion were observed between wild-type and TXNIP-deficient bone marrow-derived macrophages in response to several NLRP3 stimuli, including MSU crystals and ATP61.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [61]
In the citing paper
“However, the role of TXNIP and ROS in NLRP3 activation has been challenged.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [61]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Mechanisms linking obesity to insulin resistance and type 2 diabetes
Kahn, S. E., Hull, R. L., & Utzschneider, K. M. (2006) · Nature · doi:10.1038/nature05482 · Cited by 5,448
Self-citationGout-associated uric acid crystals activate the NALP3 inflammasome
Martinon, F., Pétrilli, V., Mayor, A., Tardivel, A., & Tschopp, J. (2006) · Nature · doi:10.1038/nature04516 · Cited by 5,326
NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals
Duewell, P., Kono, H., Rayner, K. J., Sirois, C. M., Vladimer, G., Bauernfeind, F. G., Abela, G. S., Franchi, L., Nuñez, G., Schnurr, M., et al. (2010) · Nature · doi:10.1038/nature08938 · Cited by 4,026
Self-citationTLR4 links innate immunity and fatty acid-induced insulin resistance
Shi, H., Kokoeva, M. V., Inouye, K., Tzameli, I., Yin, H., & Flier, J. S. (2006) · Journal of Clinical Investigation · doi:10.1172/jci28898 · Cited by 3,690
Bauernfeind, F. G., Horvath, G. L., Stutz, A., Alnemri, E. S., MacDonald, K. L., Speert, D. P., Fernandes‐Alnemri, T., Wu, J., Monks, B. G., Fitzgerald, K. A., et al. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0901363 · Cited by 3,087
Hornung, V., Bauernfeind, F., Halle, A., Samstad, E. O., Kono, H., Rock, K. L., Fitzgerald, K. A., & Latz, E. (2008) · Nature Immunology · doi:10.1038/ni.1631 · Cited by 3,065
Thioredoxin-interacting protein links oxidative stress to inflammasome activation
Zhou, R., Tardivel, A., Thorens, B., Choi, I., & Tschopp, J. (2010) · Nature Immunology · doi:10.1038/ni.1831 · Cited by 2,708
Innate Immune Activation Through Nalp3 Inflammasome Sensing of Asbestos and Silica
Dostert, C., Pétrilli, V., Van Bruggen, R., Steele, C., Mossman, B. T., & Tschopp, J. (2008) · Science · doi:10.1126/science.1156995 · Cited by 2,658
The NALP3 inflammasome is involved in the innate immune response to amyloid-β
Halle, A., Hornung, V., Petzold, G. C., Stewart, C. R., Monks, B. G., Reinheckel, T., Fitzgerald, K. A., Latz, E., Moore, K. J., & Golenbock, D. T. (2008) · Nature Immunology · doi:10.1038/ni.1636 · Cited by 2,441
Interleukin-1-receptor antagonist in type 2 diabetes mellitus
Larsen, C. M., Faulenbach, M., Vaag, A., Vølund, A., Ehses, J. A., Seifert, B., Mandrup-Poulsen, T., & Donath, M. Y. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa065213 · Cited by 1,798
Flagged first, then by citations
Cited by
Sorted by citations
Items 401–500 of 1,001
The Human Islet: Mini-Organ With Mega-Impact
Walker, J. T., Saunders, D. C., Briššová, M., & Powers, A. C. (2021) · Endocrine Reviews · doi:10.1210/endrev/bnab010 · Cited by 88
Foldamer-mediated manipulation of a pre-amyloid toxin
Kumar, S., Birol, M., Schlamadinger, D. E., Wojcik, S. P., Rhoades, E. R., & Miranker, A. D. (2016) · Nature Communications · doi:10.1038/ncomms11412 · Cited by 80
The role of the inflammasome in patients with autoinflammatory diseases
Hoffman, H. M., & Broderick, L. (2016) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2016.05.001 · Cited by 80
RAGE binds preamyloid IAPP intermediates and mediates pancreatic β cell proteotoxicity
Abedini, A., Cao, P., Plesner, A., Zhang, J., He, M., Derk, J., Patil, S. A., Rosario, R., Lonier, J., Song, F., et al. (2018) · Journal of Clinical Investigation · doi:10.1172/jci85210 · Cited by 83
“Activation of inflammasomes by h-IAPP aggregates triggers the production of Il1b, suggesting that Il1b enhances h-IAPP toxicity (40).”
BackgroundMicroRNAs as important regulators of the NLRP3 inflammasome
Zamani, P., Oskuee, R. K., Atkin, S. L., Navashenaq, J. G., & Sahebkar, A. (2019) · Progress in Biophysics and Molecular Biology · doi:10.1016/j.pbiomolbio.2019.05.004 · Cited by 80
Hull, R. L., Gibson, R. L., McNamara, S., Deutsch, G. H., Fligner, C. L., Frevert, C. W., Ramsey, B. W., & Sanda, S. (2018) · Diabetes Care · doi:10.2337/dc17-1387 · Cited by 79
“Given these previous observations of islet amyloidosis in CFRD (19,20), the inflammatory properties of islet amyloid (24,25), and the systemic inflammatory milieu of CF (26–28), we hypothesized that CFRD would be characterized not only by islet amyloid but also by islet ex-”
BackgroundSelf-citationInterferons and inflammasomes: Cooperation and counterregulation in disease
Labzin, L. I., Lauterbach, M., & Latz, E. (2016) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2016.05.010 · Cited by 77
Maslanik, T., Tannura, K., Mahaffey, L., Loughridge, A. B., Benninson, L., Ursell, L., Greenwood, B. N., Knight, R., & Fleshner, M. (2012) · PLoS ONE · doi:10.1371/journal.pone.0050636 · Cited by 77
“The first signal leads to synthesis of components of the inflammasome, as well as pro-IL-1b, and pro-IL-18 [71,72].”
BackgroundTargeting Inflammatory Cytokines to Improve Type 2 Diabetes Control
Velikova, T. V., Kabakchieva, P., Assyov, Y. S., & Georgiev, T. (2021) · BioMed Research International · doi:10.1155/2021/7297419 · Cited by 88
“Considerable evidence implicates tissue inflammation in pancreatic islet dysfunction, with local amyloid deposition and fibrosis leading to more severe islet inflammation [15].”
BackgroundFrom Innate Immunity to Metabolic Disorder: A Review of the NLRP3 Inflammasome in Diabetes Mellitus
Nițulescu, I. M., Ciulei, G., Cozma, A., Procopciuc, L. M., & Orasan, O. H. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12186022 · Cited by 83
“Other activators of NLRP3 in islet cells are saturated fatty acids and islet amyloid polypeptides [24,25].”
BackgroundKim, D., You, B., Lim, H., & Lee, S. J. (2011) · Molecular Pain · doi:10.1186/1744-8069-7-74 · Cited by 81
The Role of NLR-related Protein 3 Inflammasome in Host Defense and Inflammatory Diseases
Yang, C., Shin, D., & Jo, E. (2012) · International Neurourology Journal · doi:10.5213/inj.2012.16.1.2 · Cited by 81
“However, another study showed that there is no difference in IL-1β secretion between wild-type and TXNIP-deficient macrophages in response to NLRP3 stimulation [79].”
BackgroundResultInflammasome activation in obesity-related inflammatory diseases and autoimmunity.
Lukens, J. R., Dixit, V. D., & Kanneganti, T. (2011) · PubMed · Cited by 79
Islet amyloid polypeptide: Another key molecule in Alzheimer’s pathogenesis?
Zhang, Y., & Song, W. (2017) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2017.03.001 · Cited by 79
Rodríguez-Alcázar, J. F., Ataide, M. A., Engels, G., Schmitt-Mabmunyo, C., Garbi, N., Kastenmüller, W., Latz, E., & Franklin, B. S. (2018) · The Journal of Immunology · doi:10.4049/jimmunol.1800107 · Cited by 77
“The pro-inflammatory cytokine IL-1 is a key driver of crystal-induced inflammation in several chronic inflammatory diseases (Hornung et al., 2008; Duewell et al., 2010; Masters et al., 2010; Halle et al., 2008; Martinon et al., 2006b; Dostert et al., 2008).”
BackgroundZhao, G., Dharmadhikari, G., Maedler, K., & Meyer‐Hermann, M. (2014) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1003798 · Cited by 81
Shi, W., Xu, G., Zhan, X., Gao, Y., Wang, Z., Fu, S., Qin, N., Hou, X., Ai, Y., Wang, C., et al. (2020) · Cell Death and Disease · doi:10.1038/s41419-020-2460-x · Cited by 76
Dai, Z., Chen, X.-Y., An, L.-Y., Li, C., Zhao, N., Yang, F., You, S.-T., Hou, C., Li, K., Jiang, C., et al. (2020) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.0c01924 · Cited by 76
The Role of the Inflammasome in Heart Failure
Wu, J., Dong, E., Zhang, Y., & Xiao, H. (2021) · Frontiers in Physiology · doi:10.3389/fphys.2021.709703 · Cited by 78
A guide to membrane atg8ylation and autophagy with reflections on immunity
Deretic, V. P., & Lazarou, M. (2022) · The Journal of Cell Biology · doi:10.1083/jcb.202203083 · Cited by 78
Lee, H.-Y., Kim, J., Quan, W., Lee, J.-C., Kim, M., Kim, S. H., Bae, J., Hur, K. Y., & Lee, M. (2016) · Autophagy · doi:10.1080/15548627.2016.1184799 · Cited by 78
Mechanisms by which obesity impacts upon asthma
Umetsu, D. T. (2016) · Thorax · doi:10.1136/thoraxjnl-2016-209130 · Cited by 80
Sharma, B., Satija, G., Madan, A., Garg, M., Alam, M. M., Shaquiquzzaman, M., Khanna, S., Tiwari, P., Parvez, S., Iqubal, A., et al. (2022) · Inflammation · doi:10.1007/s10753-022-01730-0 · Cited by 77
“It was also observed that TXNIP is non-essential in activating the NLRP3 inflammasome when it is triggered by Aβ, monosodium urate, and ATP [112].”
BackgroundSubramanian, S. L., Hull, R. L., Zraika, S., Aston‐Mourney, K., Udayasankar, J., & Kahn, S. E. (2011) · Diabetologia · doi:10.1007/s00125-011-2338-7 · Cited by 75
“Our recent study demonstrated that fibrillar hIAPP elicits an inflammatory response (including IL-1β production) from bone marrow-derived dendritic cells and showed IL-1β co-localisation with islet amyloid deposits in vivo [36].”
BackgroundSelf-citationCurrent status of inflammasome blockers as anti-inflammatory drugs
López‐Castejón, G., & Pelegrı́n, P. (2012) · Expert Opinion on Investigational Drugs · doi:10.1517/13543784.2012.690032 · Cited by 77
“The hormone islet amyloid polypeptide has been found to be an activator of the NLRP3 inflammasome in b-cells, therefore showing a link between T2DM and NLRP3 inflammasome [56].”
BackgroundWestwell-Roper, C. Y., Chehroudi, C., Denroche, H. C., Courtade, J. A., Ehses, J. A., & Verchere, C. B. (2014) · Diabetologia · doi:10.1007/s00125-014-3447-x · Cited by 75
“While in vitro evidence suggests that interaction of hIAPP with macrophages induces release of cytokines such as IL-1β that at high local concentrations are known to cause beta cell dysfunction [10, 23], it is likely that IL-1 also plays an important physiological role in regulating islet homeostasis.”
BackgroundInfluentialControl of innate and adaptive immunity by the inflammasome
Çıracı, C., Janczy, J. R., Sutterwala, F. S., & Cassel, S. L. (2012) · Microbes and Infection · doi:10.1016/j.micinf.2012.07.007 · Cited by 75
Metabolic reprogramming & inflammation: Fuelling the host response to pathogens
Gleeson, L. E., & Sheedy, F. J. (2016) · Seminars in Immunology · doi:10.1016/j.smim.2016.10.007 · Cited by 78
Posttranslational Modification as a Critical Determinant of Cytoplasmic Innate Immune Recognition
Baker, P. J., Nardo, D. D., Moghaddas, F., Tran, L. S., Bachem, A., Nguyen, T. A., Hayman, T. J., Tye, H., Vince, J. E., Bedoui, S., et al. (2017) · Physiological Reviews · doi:10.1152/physrev.00026.2016 · Cited by 75
Self-citationLi, J.-Y., Wang, Y.-Y., Shao, T., Fan, D., Lin, A., Xiang, L., & Shao, J.-Z. (2019) · Journal of Biological Chemistry · doi:10.1074/jbc.ra119.011751 · Cited by 76
“Given that the NLRP3 inflammasome is also closely-associated with various diseases, such as type II diabetes and inflammatory bowel disease (41, 42), teleost fish will become a new research model for these kinds of diseases.”
BackgroundTarget acquired: Selective autophagy in cardiometabolic disease
Evans, T. D., Sergin, I., Zhang, X., & Razani, B. (2017) · Science Signaling · doi:10.1126/scisignal.aag2298 · Cited by 74
Duru, K. C., Kovaleva, E. G., Danilova, I. G., & van der Bijl, P. (2019) · Phytotherapy Research · doi:10.1002/ptr.6384 · Cited by 82
“Although it remains difficult to disclose which mechanism is the most crucial in a T2DM model or an individual, it is interesting to note that each of these cellular stress factors either promotes an inflammatory response or is aggravated by inflammation (Ehses, Ellingsgaard, Boni‐Schnetzler, & Donath, 2009; Masters e…”
BackgroundiGLuc: a luciferase-based inflammasome and protease activity reporter
Bartok, E., Bauernfeind, F. G., Khaminets, M. G., Jakobs, C., Monks, B. G., Fitzgerald, K. A., Latz, E., & Hornung, V. (2013) · Nature Methods · doi:10.1038/nmeth.2327 · Cited by 73
Zhang, Y., Aisker, G., Dong, H., Halemahebai, G., Zhang, Y., & Tian, L. (2021) · Phytomedicine · doi:10.1016/j.phymed.2021.153741 · Cited by 73
Westwell-Roper, C. Y., Nąckiewicz, D., Dan, M., & Ehses, J. A. (2014) · Immunology and Cell Biology · doi:10.1038/icb.2014.4 · Cited by 74
Caillon, L., Hoffmann, A. R. F., Botz, A., & Khemtémourian, L. (2015) · Journal of Diabetes Research · doi:10.1155/2016/5639875 · Cited by 74
The Inflammasome and IL-1β: Implications for the Treatment of Inflammatory Diseases
Satoh, T. K., Otsuka, A., Contassot, E., & French, L. E. (2015) · Immunotherapy · doi:10.2217/imt.14.106 · Cited by 77
Translational value of animal models of obesity—Focus on dogs and cats
Osto, M., & Lutz, T. A. (2015) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2015.03.036 · Cited by 79
“Soluble oligomers of amylin may activate the inflammasome, a multiprotein oligomer expressed in myeloid cells and components of the innate immune system, to produce proinflammatory cytokines which are toxic to β-cells (Donath and Shoelson, 2011; Masters et al., 2010).”
BackgroundInterplay between redox status and inflammasome activation
Rubartelli, A., Gattorno, M., Netea, M. G., & Dinarello, C. A. (2011) · Trends in Immunology · doi:10.1016/j.it.2011.08.005 · Cited by 73
Wang, X., Sun, B., Liu, S., & Xia, T. (2016) · NanoImpact · doi:10.1016/j.impact.2016.08.002 · Cited by 72
Lee, E. Y., Srinivasan, Y., de Anda, J., Nicastro, L. K., Tükel, Ç., & Wong, G. C. L. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.01629 · Cited by 70
“Consistent with this idea, fibrillar curli (164), Aβ (14), serum amyloid A (165), and IAPP (166) elicited IL-1β cytokine production by directly activating the NLRP3 inflammasome in macrophages.”
BackgroundMetformin selectively dampens the acute inflammatory response through an AMPK-dependent mechanism
Postler, T. S., Peng, V., Bhatt, D. M., & Ghosh, S. (2021) · Scientific Reports · doi:10.1038/s41598-021-97441-x · Cited by 73
Macrophage-targeted delivery systems for nucleic acid therapy of inflammatory diseases
Singh, A. K., Talekar, M., Raikar, A., & Amiji, M. M. (2014) · Journal of Controlled Release · doi:10.1016/j.jconrel.2014.04.021 · Cited by 73
“Presence of human islet amyloid polypeptide (IAPP) as inducer of IL-1β production bymacrophages has recently been confirmed in T2D [49].”
BackgroundNąckiewicz, D., Dan, M., Speck, M., Chow, S., Chen, Y., Pospisilik, J. A., Verchere, C. B., & Ehses, J. A. (2019) · iScience · doi:10.1016/j.isci.2019.100775 · Cited by 71
“Indeed, our own work has shown that IAPP induces IL-1b in islet macrophages and TLR ligands elevated in type 2 diabetes activate islet macrophages and have negative effects on beta-cell Ins gene expression (Nackiewicz et al., 2014;Westwell-Roper et al., 2014).”
BackgroundInfluentialZhao, M., Li, F., Jian, Y., Wang, X., Yang, H., Wang, J., Su, J., Lu, X., Xi, M., Wen, A., et al. (2020) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2020.172916 · Cited by 72
Islet Amyloid Polypeptide: A Partner in Crime With Aβ in the Pathology of Alzheimer's Disease
Raimundo, A., Ferreira, S., Martins, I. C., & Menezes, R. (2020) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2020.00035 · Cited by 74
“Chronic inflammation is also observed in local and systemic amyloidosis due to the activation of the NLRP3 inflammasome by hIAPP aggregates (Masters et al., 2010).”
BackgroundRBP–RNA interactions in the control of autoimmunity and autoinflammation
Liu, J., & Cao, X. (2023) · Cell Research · doi:10.1038/s41422-022-00752-5 · Cited by 74
Coope, A., Torsoni, A. S., & Velloso, L. A. (2016) · European Journal of Endocrinology · doi:10.1530/eje-15-1065 · Cited by 73
Gordon, E. M., Yao, X., Xu, H., Karkowsky, W., Kaler, M. M., Kalchiem‐Dekel, O., Barochia, A. V., Gao, M., Keeran, K. J., Jeffries, K. R., et al. (2019) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2019.02.027 · Cited by 70
Birnbaum, Y., Tran, D., Bajaj, M., & Ye, Y. (2019) · Basic Research in Cardiology · doi:10.1007/s00395-019-0743-0 · Cited by 71
The strategies of targeting the NLRP3 inflammasome to treat inflammatory diseases
Jiang, H., Gong, T., & Zhou, R. (2019) · Advances in immunology · doi:10.1016/bs.ai.2019.11.003 · Cited by 71
Mechanisms Underlying the Antidiabetic Activities of Polyphenolic Compounds: A Review
Nie, T., & Cooper, G. J. S. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.798329 · Cited by 75
“…leading to apoptosis (Zhang et al., 2011). hA oligomers can trigger IL-1β processing in dendritic cells and macrophages, which triggers apoptosis in β-cells (Masters et al., 2010;Westwell-Roper et al., 2014). hA-induced elevation of IL-1β levels in islets is associated with upregulation of Fas,…”
BackgroundInfluentialKapétanovic, R., Bokil, N. J., & Sweet, M. J. (2015) · Ageing Research Reviews · doi:10.1016/j.arr.2015.02.005 · Cited by 70
Methylsulfonylmethane inhibits NLRP3 inflammasome activation
Ahn, H., Kim, J., Lee, M.-J., Kim, Y. J., Cho, Y., & Lee, G. (2014) · Cytokine · doi:10.1016/j.cyto.2014.11.001 · Cited by 71
Krause, M. D. S., Bock, P. M., Takahashi, H., de Bittencourt, P. I. H., & Newsholme, P. (2015) · Clinical Science · doi:10.1042/cs20140695 · Cited by 71
Self-citationLichtnekert, J., Kulkarni, O. P., Mulay, S. R., Rupanagudi, K. V., Ryu, M., Allam, R., Vielhauer, V., Muruve, D. A., Lindenmeyer, M. T., Cohen, C. D., et al. (2011) · PLoS ONE · doi:10.1371/journal.pone.0026778 · Cited by 71
“crystals, amyloid crystals, as well as high glucose levels which render NLRP3 activation as a crucial element of a number of important inflammatory diseases such as gout, atherosclerosis, amyloidosis and diabetes [13,14,15,16].”
BackgroundAmyloid Fibrils Composed of Hexameric Peptides Attenuate Neuroinflammation
Kurnellas, M., Adams, C. M., Sobel, R. A., Steinman, L., & Rothbard, J. B. (2013) · Science Translational Medicine · doi:10.1126/scitranslmed.3005681 · Cited by 72
He, L., Wong, C. K., Cheung, K. K., Yau, H. C., Fu, A., Zhao, H., Leung, K. M., Kong, A. P., Wong, G. W., Chan, P. K., et al. (2013) · Journal of Diabetes Investigation · doi:10.1111/jdi.12063 · Cited by 70
“Control T20M Group Control T20M Group CD4+ T lymphocytes (a) (2)”
BackgroundLiu, Z., Zhao, N., Zhu, H., Zhu, S., Pan, S., Xu, J., Zhang, X., Zhang, Y., & Wang, J. (2015) · Cardiovascular Diabetology · doi:10.1186/s12933-015-0288-y · Cited by 69
“Bone marrowderived macrophages was reported also contributed in IL-1β production in diabetes [35].”
BackgroundIdentification of an ASC oligomerization inhibitor for the treatment of inflammatory diseases
Soriano‐Teruel, P. M., García‐Laínez, G., Marco-Salvador, M., Pardo, J., Arias, M. A., DeFord, C., Merfort, I., Vicent, M. J., Pelegrı́n, P., Sancho, M., et al. (2021) · Cell Death and Disease · doi:10.1038/s41419-021-04420-1 · Cited by 70
Groß, O. (2011) · Methods in molecular biology · doi:10.1007/978-1-61779-527-5_15 · Cited by 68
Cadavez, L., Montané, J., Alcarraz‐Vizán, G., Visa, M., Laia, V.-F., Servitja, J., & Novials, A. (2014) · PLoS ONE · doi:10.1371/journal.pone.0101797 · Cited by 72
“The potentiated ER stress activation in hIAPP-INS1E cells can be explained due to the increased aggregation capacity of hIAPP or the formation of intracellular oligomers, which may further affect ER stress [26,37,38].”
BackgroundTranscriptomic Network Support Distinct Roles of Classical and Non-Classical Monocytes in Human
Anbazhagan, K., Duroux-Richard, I., Jørgensen, C., & Apparailly, F. (2014) · International Reviews of Immunology · doi:10.3109/08830185.2014.902453 · Cited by 74
“The increased intracellular Ca2+ signaling and cAMP activates the NLRP inflammasome, therefore, triggering caspase-1 activation and leading to cleavage and secretion of IL-1β and IL18 into the micro-environment [61, 63].”
BackgroundCostes, S., Bertrand, G., & Ravier, M. A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22105303 · Cited by 77
“In line with these results, h-IAPP aggregation triggers activation of the NLRP3 inflammasome, leading to the production of the proinflammatory cytokine interleukin 1β (IL1β) from macrophages and dendritic cells in vitro [64] as well as from resident islet macrophages in h-IAPP transgenic mice [65,66].”
ResultTherapeutic vaccines for chronic diseases: successes and technical challenges
Bachmann, M. F., & Jennings, G. T. (2011) · Philosophical Transactions of the Royal Society B Biological Sciences · doi:10.1098/rstb.2011.0103 · Cited by 69
Lee, H. J. (2015) · World Journal of Gastroenterology · doi:10.3748/wjg.v21.i45.12787 · Cited by 68
Wallet, S. M., Puri, V., & Gibson, F. C. (2018) · Vaccines · doi:10.3390/vaccines6020021 · Cited by 69
“In addition to PAMPs [4], DAMP-mediated activation of NLRP inflammasome by self-derived molecules such as thioredoxin-interacting protein in response to glucose link endogenous oxidative stress to insulin resistance [210,211], while other DAMPs such as amylin (IAPP) activate NLRP inflammasome and IL-1 production in a…”
BackgroundFrame, J. M., Kubaczka, C., Long, T. L., Esain, V., Soto, R. A., Hachimi, M., Jing, R., Shwartz, A., Goessling, W., Daley, G. Q., et al. (2020) · Developmental Cell · doi:10.1016/j.devcel.2020.07.015 · Cited by 68
“Priming of the NLRP3 inflammasome is reliant on glycolysis and HIF1α stabilization in adult macrophages (Masters et al., 2010; Tannahill et al., 2013), and is enhanced in response to high glucose concentrations or hypoxia in mesangial cells (Tseng et al.”
BackgroundDamage-associated molecular patterns and their pathological relevance in diabetes mellitus
Shin, J. J., Lee, E. K., Park, T. J., & Kim, W. (2015) · Ageing Research Reviews · doi:10.1016/j.arr.2015.06.004 · Cited by 68
Questions and controversies in innate immune research: what is the physiological role of NLRP3?
Coll, R. C., O'Neill, L. A. J., & Schroder, K. (2016) · Cell Death Discovery · doi:10.1038/cddiscovery.2016.19 · Cited by 69
Self-citationVerma, N., Ly, H., Liu, M., Chen, J., Zhu, H., Chow, M., Hersh, L. B., & Despa, F. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160047 · Cited by 68
“Thus, incorporation of aggregated amylin in neurons in T2D patients with AD is associated with increased IL1 synthesis, consistent with the pathological role of aggregated amylin in pancreatic islets [1, 3, 4].”
BackgroundResultInfluentialThioredoxin binding protein (TBP)-2/Txnip and α-arrestin proteins in cancer and diabetes mellitus
Masutani, H., Yoshihara, E., Masaki, S., Chen, Z., & Yodoi, J. (2011) · Journal of Clinical Biochemistry and Nutrition · doi:10.3164/jcbn.11-36sr · Cited by 68
Self-citationAmbati, J., Magagnoli, J., Leung, H., Wang, S.-B., Andrews, C. A., Fu, D., Pandey, A., Sahu, S., Narendran, S., Hirahara, S., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-18528-z · Cited by 66
Bishoyi, A. K., Roham, P. H., Rachineni, K., Save, S. N., Hazari, M. A., Sharma, S., & Kumar, A. (2020) · Biological Chemistry · doi:10.1515/hsz-2020-0174 · Cited by 67
NLRP3 inflammasome inhibitor INF39 attenuated NLRP3 assembly in macrophages
Shi, Y., Lv, Q., Zheng, M., Sun, H., & Shi, F. (2021) · International Immunopharmacology · doi:10.1016/j.intimp.2020.107358 · Cited by 67
Wu, M., Lee, M. Y. Y., Bahl, V., Traum, D., Schug, J., Kusmartseva, I., Atkinson, M. A., Fan, G., & Kaestner, K. H. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.109919 · Cited by 73
“Experimental support for this model derives from rodent studies (Eguchi et al., 2012; Masters et al., 2010; Westwell-Roper et al., 2014) as well as analyses of human pancreatic samples (Ehses et al.”
NLRP3 and IL ‐1 β in macrophages as critical regulators of metabolic diseases
McGettrick, A. F., & O'Neill, L. A. J. (2013) · Diabetes Obesity and Metabolism · doi:10.1111/dom.12169 · Cited by 68
“Studies have shown that TLR4 and NLRP3 play a key role in this inflammation with TNF and IL-1β as key inflammatory cytokines [17,18].”
BackgroundInfluentialSelf-citationRole of the Inflammasome in Myocardial Infarction
Takahashi, M. (2011) · Trends in Cardiovascular Medicine · doi:10.1016/j.tcm.2012.02.002 · Cited by 66
“…silicosis, Alzheimer’s disease, atherosclerosis, and type 2 diabetes mellitus (T2DM) (Cassel et al. 2008, Chen and Nunez 2010, Davis et al. 2011, Dostert et al. 2008, Duewell et al. 2010, Halle et al. 2008, Martinon et al. 2006, Martinon et al. 2009, Masters et al. 2010, Zhou et al. 2010).”
BackgroundBezbradica, J. S., Coll, R. C., & Schroder, K. (2016) · Cellular and Molecular Immunology · doi:10.1038/cmi.2016.11 · Cited by 67
Self-citationCardiovascular diseases, NLRP3 inflammasome, and western dietary patterns
Pavillard, L. E., Marín‐Aguilar, F., Bullón, P., & Cordero, M. D. (2018) · Pharmacological Research · doi:10.1016/j.phrs.2018.03.018 · Cited by 67
The role of autophagy in endoplasmic reticulum stress-induced pancreatic β cell death
Yin, J.-J., Li, Y., Wang, Y., Liu, G., Wang, J., Zhu, X.-O., & Pan, S. (2012) · Autophagy · doi:10.4161/auto.8.2.18807 · Cited by 65
“Therefore, local cytokine production such as that of IL-1β by immune cells is involved in the pathogenesis not only of T1D, but also T2D.(34) Cytokines stimulate nitric oxide production in pancreatic β-cells, leading to the UPR, ER stress and apoptosis.”
BackgroundInfluentialBeyond the Hormone: Insulin as an Autoimmune Target in Type 1 Diabetes
Brezar, V., Carel, J., Boîtard, C., & Mallone, R. (2011) · Endocrine Reviews · doi:10.1210/er.2011-0010 · Cited by 69
Jun, H., Jung, Y.-J., & Choi, B. (2016) · Archives of Oral Biology · doi:10.1016/j.archoralbio.2016.09.010 · Cited by 66
Orlowski, G. M., Sharma, S., Colbert, J. D., Bogyo, M. S., Robertson, S. A., Kataoka, H., Chan, F. K.-M., & Rock, K. L. (2017) · Journal of Leukocyte Biology · doi:10.1189/jlb.3hi0316-152r · Cited by 65
Haneklaus, M., O’Neil, J. D., Clark, A. R., Masters, S. L., & O'Neill, L. A. J. (2017) · Journal of Biological Chemistry · doi:10.1074/jbc.m116.772947 · Cited by 66
“including type 2 diabetes, atherosclerosis, gout and Alzheimer’s disease (8-11).”
BackgroundSelf-citationProtein aggregates and proteostasis in aging: Amylin and β-cell function
Press, M., Jung, T., König, J., Grune, T., & Höhn, A. (2018) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2018.03.010 · Cited by 66
How the redox state regulates immunity
Mullen, L., Mengozzi, M., Hanschmann, E.-M., Alberts, B. M., & Ghezzi, P. (2019) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2019.12.022 · Cited by 66
Tacrolimus- and sirolimus-induced human β cell dysfunction is reversible and preventable
Dai, C., Walker, J. T., Shostak, A., Padgett, A., Spears, E., Wisniewski, S., Poffenberger, G., Aramandla, R., Dean, E. D., Prasad, N., et al. (2020) · JCI Insight · doi:10.1172/jci.insight.130770 · Cited by 64
Pyroptosis: Role and Mechanisms in Cardiovascular Disease
Chen, X., Tian, P., Wang, K., Wang, M., & Wang, K. (2022) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2022.897815 · Cited by 68
Lee, H. J., Hong, Y., Jun, W., & Yang, S. J. (2015) · Journal of Medicinal Food · doi:10.1089/jmf.2015.3439 · Cited by 63
Tanaka, T., Takahashi, K., Yamane, M., Tomida, S., Nakamura, S., Oshima, K., Niwa, A., Nishikomori, R., Kambe, N., Hara, H., et al. (2012) · Blood · doi:10.1182/blood-2012-03-417881 · Cited by 66
Inflammasomes: Key Mediators of Lung Immunity
Howrylak, J. A., & Nakahira, K. (2017) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021115-105229 · Cited by 67
Impact of Morphology on Iron Oxide Nanoparticles-Induced Inflammasome Activation in Macrophages
Liu, L., Sha, R., Yang, L., Zhao, X., Zhu, Y., Gao, J., Zhang, Y., & Wen, L. (2018) · ACS Applied Materials & Interfaces · doi:10.1021/acsami.8b17474 · Cited by 65
Survival in a bad neighborhood: pancreatic islets in cystic fibrosis
Norris, A. W., Ode, K. L., Merjaneh, L., Sanda, S., Yi, Y., Sun, X., Engelhardt, J. F., & Hull, R. L. (2019) · Journal of Endocrinology · doi:10.1530/joe-18-0468 · Cited by 64
Self-citationThe β Cell in Diabetes: Integrating Biomarkers With Functional Measures
Kahn, S. E., Chen, Y., Esser, N., Taylor, A. J., van Raalte, D. H., Zraika, S., & Verchere, C. B. (2021) · Endocrine Reviews · doi:10.1210/endrev/bnab021 · Cited by 75
“Postulated triggers of islet inflammation in type 2 diabetes, characterized by increased number of activated proinflammatory macrophages, cytokine production, and β-cell dysfunction, include dyslipidemia and IAPP aggregates (172-176).”
BackgroundSelf-citationBudden, C. F., Gearing, L. J., Kaiser, R., Standke, L., Hertzog, P. J., & Latz, E. (2021) · Journal of Extracellular Vesicles · doi:10.1002/jev2.12127 · Cited by 66
“In addition to its immuno-protective roles, activation of the NLRP3 inflammasome is increasingly recognized as a contributing factor in the pathogenesis of different inflammatory diseases (Duewell et al., 2010; Halle et al., 2008; Heneka et al., 2013; Masters et al., 2010).”
Oleszycka, E., Moran, H. B. T., Tynan, G. A., Hearnden, C. H. A., Coutts, G., Campbell, M., Allan, S. M., Scott, C. J., & Lavelle, E. C. (2015) · FEBS Journal · doi:10.1111/febs.13546 · Cited by 62
Self-citationMacrophages control innate inflammation
Akira, S., Misawa, T., Satoh, T., & Saitoh, T. (2013) · Diabetes Obesity and Metabolism · doi:10.1111/dom.12151 · Cited by 64
Alvarado, R., To, J., Lund, M. E., Pinar, A. A., Mansell, A. S., Robinson, M. W., O’Brien, B. A., Dalton, J. P., & Donnelly, S. (2016) · The FASEB Journal · doi:10.1096/fj.201500093r · Cited by 61
“Treatment of macrophages with these agents does not prevent the release of lysosomal contents into the cytosol induced by particulate material, but the resident proteases remain inactive and, therefore, incapable of activating NLRP3 (9, 10, 15).”
Son, S., Hwang, I., Han, S. H., Shin, J., Shin, O. S., & Yu, J. (2017) · Journal of Biological Chemistry · doi:10.1074/jbc.m117.806307 · Cited by 64
Metadata
- Authors
- Masters, S. L., Dunne, A., Subramanian, S. L., Hull, R. L., Tannahill, G. M., Sharp, F. A., Becker, C., Franchi, L., Yoshihara, E., Chen, Z., Mullooly, N., Mielke, L. A., Harris, J., Coll, R. C., Mills, K. H. G., Mok, K. H., Newsholme, P., Nuñez, G., Yodoi, J., Kahn, S. E., Lavelle, E. C., & O'Neill, L. A. J.
- Affiliations
- Trinity College Dublin (IE)
- University of Washington (US)
- University of Michigan (US)
- Kyoto University (JP)
- University College Dublin (IE)
- Corresponding author
- Masters, Seth L
- ORCID
- Venue
- Nature Immunology
- Published
- 2010-09-12
- Volume
- 11
- Issue
- 10
- Pages
- 897-904
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- PMC
- PMC3103663
- OpenAlex
- W2034946303
- Cited by
- 1,330
- References
- 55
- Citations by year
- 2026: 58 · 2025: 57 · 2024: 64 · 2023: 75 · 2022: 71 · 2021: 99 · 2020: 100 · 2019: 95 · 2018: 82 · 2017: 83 · 2016: 73 · 2015: 101 · 2014: 95 · 2013: 112 · 2012: 83
- FWCI
- 35.67
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion, other-oa)
- eSpace (Curtin University) (submittedVersion)
- Trinity's Access to Research Output (TARA) (Trinity College Dublin) (submittedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (AI063331, R56AI063331, R01AI063331, R37AI063331)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-75998, R01DK075998)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- NLRP3 inflammasome, amylin, IL-1β, type 2 diabetes, beta cell destruction, glibenclamide, LDL oxidation, glucose metabolism, inflammasome priming, pancreatic islets, macrophages, amyloid deposition
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Amyloid, Animals, Carrier Proteins, Cells, Cultured, Dendritic Cells, Diabetes Mellitus, Type 2, Glyburide, Humans, Hypoglycemic Agents, Islets of Langerhans, Macrophages, Mice, Inbred C57BL, Mice, Transgenic, Receptors, Cytoplasmic and Nuclear, Mice, Rats, Interleukin-1beta, Islet Amyloid Polypeptide
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
