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Mitochondrial control of the NLRP3 inflammasome
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“In humans, IL-18 blood levels increase with ageing, and strong evidence from mouse studies indicates that blockade of the NLRP3 inflammasome extends healthspan, attenuating multiple age-related degenerative changes that have been linked to inflammageing, including insulin resistance, thymic involution, T cell senescence, and bone loss as well as physical and cognitive function decline114,117,118.”
From Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty (2018) · cites this paper as [117]
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A role for mitochondria in nlrp3 inflammasome activation
Zhou, R., Yazdi, A. S., Menu, P., & Tschopp, J. (2011) · Nature · doi:10.1038/nature09663 · Cited by 5,602
Circulating mitochondrial DAMPs cause inflammatory responses to injury
Zhang, Q., Raoof, M., Chen, Y., Sumi, Y., Sursal, T., Junger, W., Brohi, K., Itagaki, K., & Hauser, C. J. (2010) · Nature · doi:10.1038/nature08780 · Cited by 3,812
Mitochondrial membrane permeabilization in cell death
Kroemer, G., Galluzzi, L., & Brenner, C. (2007) · Physiological Reviews · doi:10.1152/physrev.00013.2006 · Cited by 3,598
Self-citationSeth, R. B., Sun, L., Ea, C.-K., & Chen, Z. J. (2005) · Cell · doi:10.1016/j.cell.2005.08.012 · Cited by 3,329
Nakahira, K., Haspel, J. A., Rathinam, V. A. K., Lee, S.-J., Dolinay, T., Lam, H. C., Englert, J. A., Rabinovitch, M., Cernadas, M., Kim, H. P., et al. (2011) · Nature Immunology · doi:10.1038/ni.1980 · Cited by 3,049
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
Molecular mechanisms of necroptosis: an ordered cellular explosion
Vandenabeele, P., Galluzzi, L., Vanden Berghe, T., & Kroemer, G. (2010) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2970 · Cited by 2,382
Self-citationLoss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production
Saitoh, T., Fujita, N., Jang, M. H., Uematsu, S., Yang, B., Satoh, T., Omori, H., Noda, T., Yamamoto, N., Komatsu, M., et al. (2008) · Nature · doi:10.1038/nature07383 · Cited by 2,064
The roles of TLRs, RLRs and NLRs in pathogen recognition
Kawai, T., & Akira, S. (2009) · International Immunology · doi:10.1093/intimm/dxp017 · Cited by 1,725
Travassos, L. H., Carneiro, L. A. M., Ramjeet, M., Hussey, S., Kim, Y.-G., Magalhães, J. G., Yuan, L., Soares, F., Chea, E., Le Bourhis, L., et al. (2010) · Nature Immunology · doi:10.1038/ni.1823 · Cited by 1,306
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Self-citationInflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty
Ferrucci, L., & Fabbri, E. (2018) · Nature Reviews Cardiology · doi:10.1038/s41569-018-0064-2 · Cited by 3,690
Niikura, K., Matsunaga, T., Suzuki, T., Kobayashi, S., Yamaguchi, H., Orba, Y., Kawaguchi, A., Hasegawa, H., Kajino, K., Ninomiya, T., et al. (2013) · ACS Nano · doi:10.1021/nn3057005 · Cited by 652
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Booth, H. D. E., Hirst, W. D., & Wade-Martins, R. (2017) · Trends in Neurosciences · doi:10.1016/j.tins.2017.04.001 · Cited by 633
“One study found that mitochondrial damage occurs downstream of IL-1b and TNF-a expression [83], whereas another showed that it results in activation of the NLPR3 inflammasome [84].”
BackgroundMitophagy in human health, ageing and disease
Picca, A., Faitg, J., Auwerx, J., Ferrucci, L., & D’Amico, D. (2023) · Nature Metabolism · doi:10.1038/s42255-023-00930-8 · Cited by 635
“Cytosolic mtDNA is sensed as ‘non-self’ by pattern recognition receptors of innate immunity due to its bacterial ancestry, lack of histones and hypomethylated CpG motifs 141 .”
Mitochondrial Control of Cellular Life, Stress, and Death
Galluzzi, L., Kepp, O., Trojel‐Hansen, C., & Kroemer, G. (2012) · Circulation Research · doi:10.1161/circresaha.112.268946 · Cited by 568
“Third, mitochondrial DNA has been recently shown to be required for the optimal activation of the NLR family, pyrin domain containing 3 (NLRP3) inflammasome (a supramolecular platform catalyzing the maturation of proinflammatory interleukins, such as interleukin-1β and interleukin-18) in response to lipopolysaccharide…”
BackgroundSelf-citationMitochondrial dysfunction and the inflammatory response
López-Armada, M. J., Riveiro-Naveira, R. R., Vaamonde‐García, C., & Valcarcel‐Ares, M. N. (2013) · Mitochondrion · doi:10.1016/j.mito.2013.01.003 · Cited by 528
“Recent studies have shown mitochondria as important players in NLRP3 inflammasome activation (Green et al., 2011; Kepp et al., 2011; Nakahira et al., 2011; Shimada et al., 2012; Zhou et al., 2011).”
BackgroundInfluentialHan, Y., Xu, X., Tang, C., Gao, P., Chen, X., Xiong, X., Yang, M., Yang, S., Zhu, X., Yuan, S., et al. (2018) · Redox Biology · doi:10.1016/j.redox.2018.02.013 · Cited by 470
“Mitochondrial dysfunction has been regarded as a fundamental factor in the triggering of NLRP3mediated inflammation [16], and mtROS overproduction is a critical contributor to NLRP3 inflammasome activation [15].”
BackgroundTRPM2 links oxidative stress to NLRP3 inflammasome activation
Zhong, Z., Zhai, Y., Liang, S., Mori, Y., Han, R., Sutterwala, F. S., & Qiao, L. (2013) · Nature Communications · doi:10.1038/ncomms2608 · Cited by 374
The Metabolic Theory of Pulmonary Arterial Hypertension
Paulin, R., & Michelakis, E. D. (2014) · Circulation Research · doi:10.1161/circresaha.115.301130 · Cited by 328
“Pro-caspase-1 clustering leads to its activation via auto-processing, and active caspase-1 proteolytically cleaves a variety of cytoplasmic targets, including interleukin-1β (which is increased in PAH).(94) After an activation cascade, several other Figure 2.”
BackgroundInflammatory Bowel Disease: Mechanisms, Redox Considerations, and Therapeutic Targets
Biasi, F., Leonarduzzi, G., Oteiza, P. I., & Poli, G. (2013) · Antioxidants and Redox Signaling · doi:10.1089/ars.2012.4530 · Cited by 311
“Intact mitochondria with intense respiratory activity are necessary for NLRP3 induction, in order to control bacterial recognition and immune response (115, 240).”
Guo, W., Sun, Y., Liu, W., Wu, X., Guo, L., Cai, P., Wu, X., Wu, X., Shen, Y., Shu, Y., et al. (2014) · Autophagy · doi:10.4161/auto.28374 · Cited by 303
“The commercial ELISA kits (Dakewe, Beijing) of murine IFNG (12-2000), murine IL17A (12-2170), murine TNF (12-2720), murine IL1B (12-2012) and human IL1B (12-1012) were used to measure the cytokine levels.”
MethodThe Metabolic Basis of Pulmonary Arterial Hypertension
Sutendra, G., & Michelakis, E. D. (2014) · Cell Metabolism · doi:10.1016/j.cmet.2014.01.004 · Cited by 271
Wu, J., Yan, Z., Schwartz, D. E., Yu, J., Malik, A. B., & Hu, G. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1200860 · Cited by 265
Immune aging, dysmetabolism, and inflammation in neurological diseases
Deleidi, M., Jäggle, M., & Rubino, G. (2015) · Frontiers in Neuroscience · doi:10.3389/fnins.2015.00172 · Cited by 260
“Adipocytes secrete more than 600 bioactive molecules, which are collectively termed as adipokines and include proinflammatory mediators, such as TNF-α, monocyte chemoattractant protein (MCP)-1, and IL-6, as well as anti-inflammatory molecules (Trayhurn and Wood, 2004).”
BackgroundMitochondria in Vascular Health and Disease
Dromparis, P., & Michelakis, E. D. (2012) · Annual Review of Physiology · doi:10.1146/annurev-physiol-030212-183804 · Cited by 248
Yang, E.-J., Kim, S.-J., Kim, J. S., & Choi, I. (2012) · Biomaterials · doi:10.1016/j.biomaterials.2012.06.016 · Cited by 218
Chang, Y.-P., Ka, S., Hsu, W., Chen, A., Chao, L. K., Lin, C.-C., Hsieh, C.-C., Chen, M., Chiu, H.-W., Ho, C., et al. (2014) · Journal of Cellular Physiology · doi:10.1002/jcp.24903 · Cited by 220
“Resveratrol prevents mitochondrial damage Damaged and ROS-generating mitochondria activate the NLRP3 inflammasome (Kepp et al., 2011; Nakahira et al., 2011; Zhou et al., 2011).”
BackgroundInfluentialMitochondria as Cellular and Organismal Signaling Hubs
Shen, K., Pender, C. L., Bar‐Ziv, R., Zhang, H., Wickham, K., Willey, E., Durieux, J., Ahmad, Q., & Dillin, A. G. (2022) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev-cellbio-120420-015303 · Cited by 214
Mai, C.-T., Wu, M., Wang, C., Su, Z., Cheng, Y., & Zhang, X. (2018) · Molecular Immunology · doi:10.1016/j.molimm.2018.10.015 · Cited by 197
The inflammasome in lung diseases
dos Santos, G., Kutuzov, M. A., & Ridge, K. M. (2012) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00225.2012 · Cited by 172
“Inflammasome-regulated cytokines appear to play a major role in the development of ARDS, as demonstrated by Dolinay and colleagues (16), since increases in the levels of circulating IL-18 in critically ill patients correlate with disease severity and mortality, even after adjustment for important confounders, such as…”
BackgroundInfluentialPesticides, cognitive functions and dementia: A review
Aloizou, A., Siokas, V., Vogiatzi, C., Peristeri, E., Docea, A. O., Petrakis, D., Provatas, A., Folia, V., Chalkia, C., Vinceti, M., et al. (2020) · Toxicology Letters · doi:10.1016/j.toxlet.2020.03.005 · Cited by 164
“Additionally, the involvement of the NLPR3 inflammasome, a key component in inflammation commencement in response to ROS in neuronal damage (Kepp et al., 2011), was evinced by the elevation of IL-1b and caspase-1 in PQ-exposed mice regardless of their APP status (Chen et al.”
BackgroundPicca, A., Lezza, A. M. S., Leeuwenburgh, C., Pesce, V., Calvani, R., Bossola, M., Manes-Gravina, E., Landi, F., Bernabei, R., & Marzetti, E. (2018) · Rejuvenation Research · doi:10.1089/rej.2017.1989 · Cited by 144
“Cell death has been suggested to be another modulator of immune response through mitochondrial involvement and inflammasome activation.(51,84) Adenosine triphosphate (ATP) release following cell death has been proposed to function as a danger signal implicated in NLRP3 inflammasome activation alerting circulating neut…”
BackgroundLiu, X., Zhou, W., Zhang, X., Lü, P., Du, Q., Tao, L., Ding, Y., Wang, Y., & Hu, R. (2016) · Biochemical Pharmacology · doi:10.1016/j.bcp.2016.05.002 · Cited by 148
Ortiz, F., Acuña-Castroviejo, D., Doerrier, C., Dayoub, J. C., López, L. C., Venegas, C., García, J. A. G., López, A., Volt, H., Luna‐Sánchez, M., et al. (2014) · Journal of Pineal Research · doi:10.1111/jpi.12191 · Cited by 143
“Moreover, impaired irradiated mitochondria also release ROS to the cytosol, activating the NLRP3 inflammasome [7, 37, 45].”
BackgroundLi, Y., & Yao, H. (2016) · British Journal of Pharmacology · doi:10.1111/bph.13518 · Cited by 141
“The timely elimination of damaged, dysfunctional and aged mitochondria plays a crucial a role in preventing the release of proapoptotic proteins, mtROS and mitochondrial DNA (mtDNA), which cause apoptosis and inflammasome activation (Kepp et al., 2011; Nakahira et al., 2011; Zhou et al., 2011; Shimada et al., 2012; Al…”
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Cyclooxygenase‐2 Regulates NLRP3 Inflammasome‐Derived IL‐1β Production
Hua, K., Chou, J., Ka, S., Tasi, Y., Chen, A., Wu, S., Chiu, H., Wong, W.-T., Wang, Y., Tsai, C., et al. (2014) · Journal of Cellular Physiology · doi:10.1002/jcp.24815 · Cited by 135
“The overproduction of mitochondrial ROS promotes mitochondrial permeability and facilitates the cytosolic release of mitochondrial DNA, which stimulates activation of the NLRP3 inflammasome (Kepp et al., 2011; Zhou et al., 2011).”
BackgroundBansal, A., Rashid, C. S., Xin, F., Li, C., Polyák, E., Duemler, A., van der Meer, T., Stefaniak, M., Wajid, S., Doliba, N. M., et al. (2017) · Environmental Health Perspectives · doi:10.1289/ehp1674 · Cited by 121
“ROS can lead to the activation of NF-j B, which in turn increases pro-in fl ammatory cytokine production (Kepp et al. 2011), eventually leading to increased b -cell death and dysfunction.”
Dietary cholesterol promotes AOM-induced colorectal cancer through activating the NLRP3 inflammasome
Du, Q., Wang, Q., Fan, H., Wang, J., Liu, X., Wang, H., Wang, Y., & Hu, R. (2016) · Biochemical Pharmacology · doi:10.1016/j.bcp.2016.02.017 · Cited by 114
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Tsubouchi, K., Araya, J., & Kuwano, K. (2018) · Inflammation and Regeneration · doi:10.1186/s41232-018-0077-6 · Cited by 117
Pathophysiology of Pediatric Multiple Organ Dysfunction Syndrome
Carcillo, J. A., Podd, B. S., Aneja, R. K., Weiss, S. L., Hall, M. W., Cornell, T. T., Shanley, T. P., Doughty, L., & Nguyen, T. C. (2017) · Pediatric Critical Care Medicine · doi:10.1097/pcc.0000000000001052 · Cited by 110
Oh, J. Y., Ko, J. H., Lee, H. J., Yu, J. M., Choi, H., Kim, M. K., Wee, W. R., & Prockop, D. J. (2014) · Stem Cells · doi:10.1002/stem.1608 · Cited by 125
Chen, L., Na, R., Boldt, E., & Ran, Q. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.05.018 · Cited by 112
“NLRP3 inflammasome plays a key role in sensingmitochondrial stress such as increased ROS (Kepp et al., 2011; Zhou et al., 2011).”
BackgroundC dk5‐ D ependent A ctivation of N euronal I nflammasomes in P arkinson's D isease
Zhang, P., Shao, X., Qi, G., Chen, Q., Bu, L.-L., Chen, L., Shi, J., Ming, J., & Tian, B. (2016) · Movement Disorders · doi:10.1002/mds.26488 · Cited by 102
“Recently, considerable evidence has indicated that excessive ROS generation and mtDNA release by mitochondria promote the activation of inflammasomes in multiple diseases such as rheumatoid arthritis (RA), lung disease, infectious diseases, and Alzheimer’s disease (AD).(9-13) PD has also generally been considered a me…”
BackgroundAswani, A. D., Manson, J., Itagaki, K., Chiazza, F., Collino, M., Wupeng, W. L., Chan, T. K., Wong, W. S. F., Hauser, C. J., Thiemermann, C., et al. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00891 · Cited by 102
“Appearance in T-HS Trauma hemorrhagic shock leads to cellular stress, failure of mitophagy, and autophagy, increasing degrees of oxidative stress, translocation of mtDNA to the cytosol, and activation of apoptotic cell death pathways (49, 50).”
BackgroundLiao, P., Chao, L. K., Chou, J., Dong, W.-C., Lin, C.-N., Lin, C.-Y., Chen, A., Ka, S., Ho, C., & Hua, K. (2012) · Inflammation Research · doi:10.1007/s00011-012-0555-2 · Cited by 97
“In addition to NADPH oxidase, mitochondria are the important source of ROS in cells and control the activation of NLRP3 inflammasome [33, 34].”
STAT3/Mitophagy Axis Coordinates Macrophage NLRP3 Inflammasome Activation and Inflammatory Bone Loss
Zhu, L., Wang, Z., Sun, X., Yu, J., Li, T., Zhao, H., Ji, Y., Peng, B., & Du, M. (2020) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.4756 · Cited by 104
“Autophagic clearance of defective mitochondria throughmitophagy is a negativemodulator of the NLRP3 inflammasome activation.((47,54)) Interestingly, a recent report demonstrates that targeting STAT3 in intestinal epithelial cells promotes PINK1 and Parkin RBR E3 ubiquitin-protein ligase (Parkin)-dependent mitophagy.”
BackgroundMKK3 regulates mitochondrial biogenesis and mitophagy in sepsis-induced lung injury
Mannam, P., Shinn, A. S., Srivastava, A., Neamu, R., Walker, W. E., Bohanon, M. J., Merkel, J., Kang, M., Cruz, C. S. D., Ahasic, A. M., et al. (2014) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00272.2013 · Cited by 97
“Mitochondria are mediators of inflammatory responses (19, 54) and become dysfunctional in sepsis and lung injury (4, 6), suggesting they are involved in the observed pathology.”
Mitochondrial redox system, dynamics, and dysfunction in lung inflammaging and COPD
Lerner, C. A., Sundar, I. K., & Rahman, I. (2016) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2016.07.026 · Cited by 96
“on the cell surface, or are present in the cytoplasm, leading to inflammasome activation (Kepp et al., 2011).”
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Lenders, V., Koutsoumpou, X., Sargsian, A., & Manshian, B. B. (2020) · Nanoscale Advances · doi:10.1039/d0na00478b · Cited by 93
Jang, Y., Lee, A. Y., Jeong, S., Park, K.-H., Paik, M.-K., Cho, N.-J., Kim, J., & Cho, M. (2015) · Toxicology · doi:10.1016/j.tox.2015.09.006 · Cited by 88
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Self-citationZhuang, Y., Ding, G., Zhao, M., Bai, M., Yang, L., Ni, J., Wang, R., Jia, Z., Huang, S., & Zhang, A. (2014) · Journal of Biological Chemistry · doi:10.1074/jbc.m114.578260 · Cited by 86
“Mitochondria are complex intracellular organelles that are involved in many metabolic circuitries, such as energy production, reactive oxygen species (ROS)(2) generation, and calcium homeostasis, and in signaling transduction pathways, such as cell death pathways (8).”
BackgroundMicroRNA-Regulated Proinflammatory Cytokines in Sarcopenia
Fan, J., Kou, X., Yang, Y., & Chen, N. (2016) · Mediators of Inflammation · doi:10.1155/2016/1438686 · Cited by 98
“Dysfunctional mitochondria are able to modulate aging-related inflammatory processes through direct activation of NLRP3 inflammasome, which can correspondingly result in the activation of caspase-1 or redox-sensitive inflammatory signaling pathways, thus leading to the production of IL-1𝛽 and IL-18 [19, 20].”
BackgroundManevski, M., Muthumalage, T., Devadoss, D., Sundar, I. K., Wang, Q., Singh, K. P., Unwalla, H. J., Chand, H. S., & Rahman, I. (2020) · Redox Biology · doi:10.1016/j.redox.2020.101443 · Cited by 87
“lated mtROS and mtDNA release, which could cause inflammation and apoptosis [225,226].”
BackgroundZhuang, Y., Yasinta, M., Hu, C., Zhao, M., Ding, G., Bai, M., Yang, L., Ni, J., Wang, R., Jia, Z., et al. (2015) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00203.2014 · Cited by 82
“Mitochondria are the major source of ROS production in live cells and contribute to Ca(2) homeostasis and signal transduction (10).”
BackgroundValcarcel‐Ares, M. N., Riveiro-Naveira, R. R., Vaamonde‐García, C., Loureiro, J., Hermida-Carballo, L., Blanco, F. J., & López-Armada, M. J. (2014) · Rheumatology · doi:10.1093/rheumatology/keu016 · Cited by 86
Nishi, Y., Satoh, M., Nagasu, H., Kadoya, H., Ihoriya, C., Kidokoro, K., Sasaki, T., & Kashihara, N. (2013) · Kidney International · doi:10.1038/ki.2012.475 · Cited by 81
CFTR activity and mitochondrial function
Valdivieso, Á. G., & Santa-Coloma, T. A. (2013) · Redox Biology · doi:10.1016/j.redox.2012.11.007 · Cited by 83
“modulating the inflammasome-mediated production of proinflammatory cytokines [298].”
BackgroundNickel Induces Interleukin-1β Secretion via the NLRP3–ASC–Caspase-1 Pathway
Li, X., & Zhong, F. (2013) · Inflammation · doi:10.1007/s10753-013-9759-z · Cited by 78
Pulmonary Arterial Hypertension: Challenges in Translational Research and a Vision for Change
Sutendra, G., & Michelakis, E. D. (2013) · Science Translational Medicine · doi:10.1126/scitranslmed.3005428 · Cited by 82
“(iii) Although yet unexplored in PAH, mitochondrial suppression may also activate the inflammasome (59), which could cause a cascade of events that increases autocrine or paracrine cytokines (60) and recruits inflammatory cells to the diseased pulmonary circulation (61).”
BackgroundAutophagy in the cancer-immunity dialogue
Yamazaki, T., Pedro, J. M. B., Galluzzi, L., Kroemer, G., & Pietrocola, F. (2020) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2020.12.003 · Cited by 80
Self-citationMacrophage inflammasome mediates hyperhomocysteinemia-aggravated abdominal aortic aneurysm
Sun, W., Pang, Y., Liu, Z., Sun, L., Liu, B., Xu, M., Dong, Y., Feng, J., Jiang, C., Kong, W., et al. (2015) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2015.02.005 · Cited by 76
“Macrophage NLRP3 inflammasome activation is specifically mediated by mitochondrial ROS, as reported in a series of recent investigations [25–27].”
Guo, W., Liu, W., Jin, B., Geng, J., Li, J., Ding, H., Wu, X., Xu, Q., Sun, Y., & Gao, J. (2015) · International Immunopharmacology · doi:10.1016/j.intimp.2014.12.009 · Cited by 76
Mangiferin from Pueraria tuberosa reduces inflammation via inactivation of NLRP3 inflammasome
Bulugonda, R. K., kumar, K. A., Gangappa, D., Beeda, H., Philip, G. H., Muralidhara Rao, D., & Faisal, S. M. (2017) · Scientific Reports · doi:10.1038/srep42683 · Cited by 74
Chiu, H., Li, L.-H., Hsieh, C., Rao, Y. K., Chen, F.-H., Chen, A., Ka, S., & Hua, K. (2019) · Scientific Reports · doi:10.1038/s41598-019-42130-z · Cited by 68
Inflammation links ageing to the brain
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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
Rath, E., & Haller, D. (2011) · Inflammatory Bowel Diseases · doi:10.1002/ibd.21944 · Cited by 55
“bind MAVS, subsequently leading to activation of interferon-regulatory factors (IRF) and nuclear factor kappaB (NF-jB), and downstream to the production of IFN as well as proinflammatory cytokines.(27,115) Notably, with regard to mtUPR-induced PKR activation, PKR has also been shown”
BackgroundPersistent Mitochondrial Dysfunction Linked to Prolonged Organ Dysfunction in Pediatric Sepsis
Weiss, S. L., Zhang, D. “., Bush, J., Graham, K., Starr, J. P., Tuluc, F., Henrickson, S. E., Kilbaugh, T. J., Deutschman, C. S., Murdock, D. G., et al. (2019) · Critical Care Medicine · doi:10.1097/ccm.0000000000003931 · Cited by 54
“It is possible that our early measurements reflect an acute rise damaged mitochondria which, resembling bacterial DNA, contribute to inflammation and cellular dysfunction, as previously observed (27, 39, 40).”
BackgroundResultThe Impact of Mitochondrial Deficiencies in Neuromuscular Diseases
Cantó, J., Grau‐Junyent, J. M., & Garrabou, G. (2020) · Antioxidants · doi:10.3390/antiox9100964 · Cited by 54
“Once in complex IV, electrons are transferred to molecular oxygen, producing water [7,95].”
BackgroundMitochondria break free: Mitochondria-derived vesicles in aging and associated conditions
Ferrucci, L., Guerra, F., Bucci, C., Marzetti, E., & Picca, A. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102549 · Cited by 58
“Owing to the lack of histones and the presence of hypomethylated CpG motifs, cell-free mtDNA can bind to a set of receptors of innate immunity and trigger inflammation, probably because of its resemblance to bacterial DNA (Kepp et al., 2011).”
BackgroundRole of glial cells in innate immunity and their role in CNS demyelination
Sriram, S. (2011) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2011.08.012 · Cited by 52
NLRP inflammasome as a key role player in the pathogenesis of environmental toxicants
Moloudizargari, M., Moradkhani, F., Asghari, N., Fallah, M., Asghari, M. H., Moghadamnia, A. A., & Abdollahi, M. R. (2019) · Life Sciences · doi:10.1016/j.lfs.2019.116585 · Cited by 53
Li, D. X., Yang, S., Xing, Y., Pan, L., Zhao, R., Zhao, Y., Liu, L., & Wu, M. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.673839 · Cited by 50
Role of mitochondrial dysfunction on rheumatic diseases
Vaamonde‐García, C., & López-Armada, M. J. (2019) · Biochemical Pharmacology · doi:10.1016/j.bcp.2019.03.008 · Cited by 45
Hua, K., Yang, F., Chiu, H., Chou, J., Dong, W.-C., Lin, C.-N., Lin, C.-Y., Wang, J., Li, L.-H., Chiu, H.-W., et al. (2015) · Infection and Immunity · doi:10.1128/iai.00125-15 · Cited by 46
The influence of oxidative stress and autophagy cross regulation on pregnancy outcome
Ramos, B. R. D. A., & Witkin, S. S. (2016) · Cell Stress and Chaperones · doi:10.1007/s12192-016-0715-3 · Cited by 46
Endothelial MKK3 Is a Critical Mediator of Lethal Murine Endotoxemia and Acute Lung Injury
Mannam, P., Zhang, X., Shan, P., Zhang, Y., Shinn, A. S., Zhang, Y., & Lee, P. J. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1202012 · Cited by 42
“New evidence suggests that mitochondria play a critical role in inflammatory responses (32, 33).”
BackgroundReduced mitochondrial activity in colonocytes facilitates AMPKα2‐dependent inflammation
Heller, S., Penrose, H. M., Cable, C., Biswas, D., Nakhoul, H. N., Baddoo, M., Flemington, E. F., Crawford, S. E., & Savkovic, S. D. (2017) · The FASEB Journal · doi:10.1096/fj.201600976r · Cited by 43
“Additionally, IBD pathophysiology is driven by extensive mucosal injury due to infiltrated inflammatory cells, leading to elevated ROS (6, 9, 10), which could trigger inflammasome-mediated cytokine production (11, 12).”
BackgroundYang, S., Hsu, W., Wu, C.-Y., Shang, H., Liu, F., Chen, A., Hua, K., & Ka, S. (2020) · The FASEB Journal · doi:10.1096/fj.202001326r · Cited by 42
Mitochondrial Dysfunction: Metabolic Drivers of Pulmonary Hypertension
Suliman, H. B., & Nozik‐Grayck, E. (2019) · Antioxidants and Redox Signaling · doi:10.1089/ars.2018.7705 · Cited by 38
“Although inflammatory cytokines can suppress mitochondrial function, mitochondria themselves can activate the NLPR3 (NACHT, LRR, and PYD domains-containing protein 3) inflammasome (66), leading to a cascade that results in increased levels of lungs and circulation inflammatory cytokines in patients with PH (36).”
BackgroundEsteves, A. R., Silva, D. F., Banha, D., Candeias, E., Guedes, B., & Cardoso, S. M. (2023) · Redox Biology · doi:10.1016/j.redox.2023.102714 · Cited by 38
“chondrial outer membrane, stimulate activation of the nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3 (NLRP3) inflammasome and the production of IL-1β and IL-18 [16].”
BackgroundWu, M., Li, S., Yu, X., Chen, W., Ma, H., Shao, C., Zhang, Y., Zhang, A., Huang, S., & Jia, Z. (2019) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00076.2019 · Cited by 38
“Mitochondria serve as a key regulatory hub of multiple cellular processes (12, 20, 26, 32, 46).”
BackgroundAn, X., Sun, X., Yang, X., Liu, D., Hou, Y., Chen, H., & Wu, J. (2019) · Artificial Cells Nanomedicine and Biotechnology · doi:10.1080/21691401.2019.1652631 · Cited by 34
Guerville, F., Vialemaringe, M., Cognet, C., Duffau, P., Lazaro, E., Cazanave, C., Bonnet, F., Leleux, O., Rossignol, R., Pinson, B., et al. (2023) · AIDS · doi:10.1097/qad.0000000000003546 · Cited by 36
“appearance of oxidative stress, known as the main metabolic event associated with NLRP3 inflammasome assembly [66,67].”
BackgroundBelicha‐Villanueva, A., Riddell, J. R., Bangia, N., & Gollnick, S. O. (2012) · Lasers in Surgery and Medicine · doi:10.1002/lsm.21160 · Cited by 34
“HPPH localizes to the mitochondrial membrane [41]; mitochondrial damage or stress can lead to NF-kB activation and cytokine secretion [42], which may lead to increases in MICA expression [16,23].”
BackgroundThe Significance of NLRP Inflammasome in Neuropsychiatric Disorders
Shen, Y., Qian, L., Luo, H., Li, X., Ruan, Y., Fan, R., Si, Z., Chen, Y.-P., Li, L., & Liu, Y. (2022) · Brain Sciences · doi:10.3390/brainsci12081057 · Cited by 32
“Studies on neuropsychiatric disorders primarily focus on NLRP1 and NLRP3 inflammasome [9].”
BackgroundYao, H. H., Zhang, Y., Liu, L., Xu, Y., Liu, X., Lin, J., Zhou, W., Wei, P., Jin, P., & Wen, L. (2016) · Biomaterials · doi:10.1016/j.biomaterials.2016.08.036 · Cited by 31
Zhuang, J., Wen, X., Zhang, Y.-Q., Shan, Q., Zhang, Z.-F., Zheng, G., Fan, S., Li, M., Wu, D., Hu, B., et al. (2017) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2017.05.014 · Cited by 30
“In addition, western blotting confirmed the ability of the NLRP3 shRNA lentivirus to reduce NLRP3 levels, as well as the production of active caspase 1 and active IL-1β in the mouse hippocampus compared with that of the Scrambled group (Supplementary Figs.”
InfluentialLi, L.-H., Lin, J.-S., Chiu, H., Lin, W.-Y., Ju, T., Chen, G. T. Y., Chernikov, O. V., Liu, M.-L., Chang, J.-C., Hsu, C.-H., et al. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.01815 · Cited by 32
“K efflux triggers downstream signaling and leads to mitochondrial damage, thereby activating the NLRP3 inflammasome (23, 24).”
BackgroundZhang, Z., Cheng, X., Li, Y., Cui, W., Zhou, W., Gao, J., & Yao, H. (2017) · Journal of Cellular Physiology · doi:10.1002/jcp.25844 · Cited by 30
Wu, D., Zhang, H., Li, F., Liu, S., Wang, Y., Zhang, Z., Wang, J., & Wu, Q. (2024) · Biochimica et Biophysica Acta (BBA) - General Subjects · doi:10.1016/j.bbagen.2024.130612 · Cited by 31
Lei, X., Li, S., Luo, C., Wang, Y., Liu, Y., Xu, Z., Huang, Q., Zou, F., Chen, Y., Peng, F., et al. (2020) · Mediators of Inflammation · doi:10.1155/2020/3934769 · Cited by 29
Chao, L. K., Lin, C., Chiu, H.-W., Wong, W.-T., Chiu, H., Tasi, Y., Kuo, Y., Chiu, Y.-C., Liu, M.-L., Ho, C., et al. (2015) · Journal of Agricultural and Food Chemistry · doi:10.1021/jf5054436 · Cited by 29
Park, G., Moon, B. C., Ryu, S. M., Kim, W. J., & Lim, H.-S. (2021) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2021/8878153 · Cited by 29
“ROS may lead to programmed cell death, by increasing the cytosolic concentration of proapoptotic factors, but are also crucial NLRP3 inflammasome activators [44, 45].”
BackgroundLiu, W., Yang, J., Fang, S., Jiao, C., Gao, J., Zhang, A., Wu, T., Tan, R. X., Xu, Q., & Guo, W. (2022) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2022.102696 · Cited by 28
“8A specifically targets ASC It is well established that mitochondrial dysfunction, exemplified by the overproduction of ROS, is essential for the assembly of the NLRP3 inflammasome (18,19).”
BackgroundVarga, A., Budai, M. M., Milesz, S., Bácsi, A., Tőzsér, J., & Benkő, S. (2012) · Immunology · doi:10.1111/imm.12052 · Cited by 27
Ho, L., Hossen, M. N., Nguyen, T. B., Vo, A., & Ahsan, F. (2022) · Biomedicines · doi:10.3390/biomedicines10010170 · Cited by 27
Immunogenic Cell Death Driven by Radiation—Impact on the Tumor Microenvironment
Yamazaki, T., Vanpouille‐Box, C., Demaria, S., & Galluzzi, L. (2020) · Cancer treatment and research · doi:10.1007/978-3-030-38862-1_10 · Cited by 28
Self-citationImplication of the NLRP3 Inflammasome in Bovine Age-Related Sarcopenia
Biase, D. D., Piegari, G., Prisco, F., Cimmino, I., d’Aquino, I., Baldassarre, V., Oriente, F., Papparella, S., & Paciello, O. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22073609 · Cited by 24
“Real-Time RT-PCR Analysis Changes of TNF-α, IL-1β and IL-18 levels in skeletal muscle were measured with RT- PCR analysis.”
BackgroundInfluentialLung Pneumonitis and Fibrosis in Cancer Therapy: A Review on Cellular and Molecular Mechanisms
Xu, C., Najafi, M., & Shang, Z. (2022) · Current Drug Targets · doi:10.2174/1389450123666220907144131 · Cited by 25
The Causal Role of Mitochondrial Dynamics in Regulating Innate Immunity in Diabetes
Chang, Y., Lin, H., Shen, F., Su, Y., Chuang, J., Lin, T., Liou, C., Lin, C., Weng, S., & Wang, P. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.00445 · Cited by 23
“Mitochondrial dysfunction has been regarded as a fundamental factor in the triggering of NLRP3-mediated inflammation (12), and mitochondrial reactive oxygen species (ROS) overproduction is critical for activation of NLRP3 inflammasome (13).”
BackgroundYamazaki, T., Yamada, S., Ohshio, K., Sugamata, M., & Morita, Y. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23031443 · Cited by 24
“Damaged mitochondria generate ROS, leading to oxidative stress and inflammatory response in cells [27].”
BackgroundHe, C., Liu, J., Li, J., Wu, H., Jiao, C., Ze, X., Xu, S., Zhu, Z., Guo, W., Xu, J., et al. (2024) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.4c00504 · Cited by 23
Does Inflammation Contribute to Cancer Incidence and Mortality during Aging? A Conceptual Review
Guerville, F., Bourdel‐Marchasson, I., Déchanet‐Merville, J., Pellegrin, I., Soubeyran, P., Appay, V., & Lemoine, M. (2022) · Cancers · doi:10.3390/cancers14071622 · Cited by 25
“Furthermore, mitochondrial dysfunction is involved in inflammasome activation following various stimuli [83].”
BackgroundAstrogliopathy and oligodendrogliopathy are early events in CNS demyelination
Zhang, F., Yao, S., Whetsell, W. O., & Sriram, S. (2013) · Glia · doi:10.1002/glia.22513 · Cited by 21
“…the retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) are among the main pathogen recognition receptors which play a fundamental role in mediating an efficient immune response to microorganisms (Akira, 2003; Bielig et al., 2011; Kepp et al., 2011; Lam- kanfi, 2011; Shaw et al., 2011).”
BackgroundImmunomodulatory Effects of Danshen (Salvia miltiorrhiza) in BALB/c Mice
Gao, D., Mendoza, A., Lu, S., & Lawrence, D. A. (2012) · ISRN Inflammation · doi:10.5402/2012/954032 · Cited by 19
“Recently, the published data suggest that mitochondria are involved in innate immune response [58, 59].”
BackgroundKianpour, F., Mohseni, M., Beigmohamadi, M., Yazdinezhad, A., Ramazani, A., Hosseini, M.-J., & Sharafi, A. (2021) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2021.113959 · Cited by 18
Metadata
- Authors
- Kepp, O., Galluzzi, L., & Kroemer, G.
- Affiliations
- Université Paris-Sud (FR)
- Inserm (FR)
- Corresponding author
- Kroemer, Guido
- Venue
- Nature Immunology
- Published
- 2011-02-15
- Volume
- 12
- Issue
- 3
- Pages
- 199-200
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- OpenAlex
- W1981120301
- Cited by
- 168
- References
- 12
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 10 · 2023: 8 · 2022: 16 · 2021: 9 · 2020: 17 · 2019: 12 · 2018: 8 · 2017: 12 · 2016: 14 · 2015: 10 · 2014: 12 · 2013: 16 · 2012: 11
- FWCI
- 5.72
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- mitochondria, NLRP3 inflammasome, innate immunity, inflammatory cytokines, inflammasome regulation, mitochondrial function
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Carrier Proteins, Humans, Immunity, Innate, Mitochondria, Models, Biological, Signal Transduction, Cytokines, Inflammasomes
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