The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Circulating mitochondrial DAMPs cause inflammatory responses to injury
Open accessAbstract
Injury causes a systemic inflammatory response syndrome (SIRS) that is clinically much like sepsis. Microbial pathogen-associated molecular patterns (PAMPs) activate innate immunocytes through pattern recognition receptors. Similarly, cellular injury can release endogenous 'damage'-associated molecular patterns (DAMPs) that activate innate immunity. Mitochondria are evolutionary endosymbionts that were derived from bacteria and so might bear bacterial molecular motifs. Here we show that injury releases mitochondrial DAMPs (MTDs) into the circulation with functionally important immune consequences. MTDs include formyl peptides and mitochondrial DNA. These activate human polymorphonuclear neutrophils (PMNs) through formyl peptide receptor-1 and Toll-like receptor (TLR) 9, respectively. MTDs promote PMN Ca(2+) flux and phosphorylation of mitogen-activated protein (MAP) kinases, thus leading to PMN migration and degranulation in vitro and in vivo. Circulating MTDs can elicit neutrophil-mediated organ injury. Cellular disruption by trauma releases mitochondrial DAMPs with evolutionarily conserved similarities to bacterial PAMPs into the circulation. These signal through innate immune pathways identical to those activated in sepsis to create a sepsis-like state. The release of such mitochondrial 'enemies within' by cellular injury is a key link between trauma, inflammation and SIRS.
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
“these organelles express biomolecules that resemble those expressed by prokaryotes, such as cardiolipin, double-stranded-hypomethylated DNA and N-formylated peptides12,13”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [13]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In human neutrophils, the binding of FPR1 and FPR2 to N-formylated peptides triggers the release of Ca2+ into the cytosol and ultimately leads to the migration and activation of neutrophils13”
From The role of mitochondria in rheumatic diseases (2022) · cites this paper as [13]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Mitochondria are considered as deriving from the endosymbiosis of an α-synfular; proteobacterium (3, 4), providing the organelles many bacterial features (3, 5–9).”
From Autoantibodies in Systemic Lupus Erythematosus Target Mitochondrial RNA (2019) · cites this paper as [9]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Cardiolipin, N-formylated peptides, mtDNA, ATP and reactive oxygen species are known mitochondrial damage-associated molecular patterns (9, 28–30).”
From Autoantibodies in Systemic Lupus Erythematosus Target Mitochondrial RNA (2019) · cites this paper as [9]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Mitochondrial debris were observed in blood in the Twin Study (Garrett-Bakelman et al., 2019) and mitochondrial damage-associated molecular patterns (DAMPs) activate innate immune pathways (Banoth and Cassel, 2018; Zhang et al., 2010).”
From Comprehensive Multi-omics Analysis Reveals Mitochondrial Stress as a Central Biological Hub for Spaceflight Impact (2020) · cites this paper as Zhang et al., 2010
The cited source says what the claim attributes to it.
In the citing paper
“In an extreme example such as massive trauma, mito-DAMPs, identified as mtDNA and formyl peptides, are acutely released from damaged tissues and cause a sepsis-like systemic inflammatory response syndrome by activating polymorphonuclear cells via TLR9 and formyl peptide receptor-129.”
From Hepatocyte mitochondria-derived danger signals directly activate hepatic stellate cells and drive progression of liver fibrosis (2020) · cites this paper as [29]
The cited source says what the claim attributes to it.
In the citing paper
“Like bacteria, mitochondria are formed of an outer and an inner membrane (inner contains cardiolipin)4,5, express formylated peptides6,7, and contain a circular genome with hypomethylated DNA CpG motifs, referred to as mitochondrial DNA (mtDNA)8,9.”
From Anti-mitochondrial autoantibodies in systemic lupus erythematosus and their association with disease manifestations (2019) · cites this paper as [6]
The cited source says what the claim attributes to it.
In the citing paper
“Mitochondria and their components (e.g. N-formylated peptides and mtDNA) are recognized as damage-associated molecular patterns (DAMPs), which activate the innate immune system and elicit an inflammatory response6,21–23.”
From Anti-mitochondrial autoantibodies in systemic lupus erythematosus and their association with disease manifestations (2019) · cites this paper as [6]
In the citing paper
“MtDNA has been reported to activate immunity through two distinct pathways, namely Toll-like receptor 9 (TLR9; Zhang et al, 2010;Oka et al, 2012;Liu et al, 2015), and cGAS activation (White et al, 2014;West et al, 2015).”
From Mitochondrial DNA and TLR9 drive muscle inflammation upon Opa1 deficiency (2018) · cites this paper as Zhang et al, 2010
In the citing paper
“Mitochondria are a source of damage-associated molecular patterns (DAMPs), and among others, mtDNA has been shown to induce a pro-inflammatory state (Zhang et al, 2010;Oka et al, 2012;Wenceslau et al, 2014).”
From Mitochondrial DNA and TLR9 drive muscle inflammation upon Opa1 deficiency (2018) · cites this paper as Zhang et al, 2010
In the citing paper
“MtDNA is recognized as foreign when found outside of mitochondria and can trigger inflammation (Maekawa et al., 2019; Shimada et al., 2012; Zhang et al., 2010).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Zhang et al., 2010
In the citing paper
“mtDNA is known to localize to endosomes”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Zhang et al., 2010
In the citing paper
“activate DNA sensor and pro-inflammatory mediator TLR9 (Zhang et al., 2010)”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Zhang et al., 2010
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
Baker, S. P., O’Neill, B., Haddon, W. F., & Long, W. B. (1974) · PubMed · Cited by 7,946
Mizgerd, J. P., Kubo, H., Kutkoski, G. J., Bhagwan, S. D., Scharffetter-Kochanek, K., Beaudet, A. L., & Doerschuk, C. M. (1997) · The Journal of Experimental Medicine · doi:10.1084/jem.186.8.1357 · Cited by 7,332
Baker, S. P., O’Neill, B., Haddon, W. F., & Long, W. B. (1974) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/00005373-197403000-00001 · Cited by 7,326
Tolerance, Danger, and the Extended Family
Matzinger, P. (1994) · Annual Review of Immunology · doi:10.1146/annurev.iy.12.040194.005015 · Cited by 4,848
Approaching the asymptote? Evolution and revolution in immunology.Preprint
Janeway, C. (1989) · Cold Spring Harbor Symposia on Quantitative Biology · doi:10.1101/sqb.1989.054.01.003 · Cited by 3,396
On the origin of mitosing cells
Sagan, L. (1967) · Journal of Theoretical Biology · doi:10.1016/0022-5193(67)90079-3 · Cited by 1,870
The mitochondrial genome: structure, transcription, translation and replication
Taanman, J.-W. (1999) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/s0005-2728(98)00161-3 · Cited by 1,635
Seong, S., & Matzinger, P. (2004) · Nature reviews. Immunology · doi:10.1038/nri1372 · Cited by 1,224
Toll-like receptors stimulate human neutrophil function
Hayashi, F., Means, T. K., & Luster, A. D. (2003) · Blood · doi:10.1182/blood-2003-04-1078 · Cited by 939
N-formylmethionyl peptides as chemoattractants for leucocytes.
Schiffmann, E., Corcoran, B. A., & Wahl, S. M. (1975) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.72.3.1059 · Cited by 889
Flagged first, then by citations
Cited by
Sorted by citations
Items 801–900 of 1,018
RYKOVA, E. Y., Sizikov, A. E., Roggenbuck, D., Antonenko, O. V., Bryzgalov, L. O., Morozkin, E. S., Skvortsova, K., Vlassov, V. V., Laktionov, P. P., & Va, K. (2017) · Arthritis Research & Therapy · doi:10.1186/s13075-017-1295-z · Cited by 87
New and revisited approaches to preserving the reperfused myocardium
Kloner, R. A., Brown, D. A., CSETE, M. E., Dai, W., Downey, J. M., Gottlieb, R. A., Hale, S. L., & Shi, J. (2017) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2017.102 · Cited by 86
Characterization and origins of cell-free mitochondria in healthy murine and human blood
Stephens, O. R., Grant, D., Frimel, M., Wanner, N., Yin, M., Willard, B. B., ERZURUM, S. C., & Asosingh, K. (2020) · Mitochondrion · doi:10.1016/j.mito.2020.08.002 · Cited by 81
Role of released mitochondrial DNA in acute lung injury
Long, G., Gong, R., Wang, Q., Zhang, D., & Huang, C. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.973089 · Cited by 83
Long-term human spaceflight and inflammaging: Does it promote aging?
Capri, M., Conte, M., Ciurca, E., Pirazzini, C., Garagnani, P., Santoro, A., Longo, F., Salvioli, S., Lau, P., Moeller, R., et al. (2023) · Ageing Research Reviews · doi:10.1016/j.arr.2023.101909 · Cited by 88
Mitochondrial Dysfunction in Cardiovascular Diseases
Yang, H. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26051917 · Cited by 91
Carbon monoxide negatively regulates NLRP3 inflammasome activation in macrophages
Jung, S. S., Moon, J., Xu, J., Ifedigbo, E., Ryter, S. W., Choi, A. M. K., & Nakahira, K. (2015) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00400.2014 · Cited by 84
Redox signaling mediated by the gut microbiota
Neish, A. S. (2013) · Free Radical Research · doi:10.3109/10715762.2013.833331 · Cited by 83
Balasubramanian, K., Maeda, A., Lee, J. S., Mohammadyani, D., Dar, H. H., Jiang, J. F., Croix, C. M. S., Watkins, S. C., Tyurin, V. A., Tyurina, Y. Y., et al. (2015) · Science Signaling · doi:10.1126/scisignal.aaa6179 · Cited by 82
Toll-Like Receptor Signaling in Burn Wound Healing and Scarring
D’Arpa, P., & Leung, K. P. (2017) · Advances in Wound Care · doi:10.1089/wound.2017.0733 · Cited by 84
FPR1 is the plague receptor on host immune cells
Osei‐Owusu, P., Charlton, T. M., Kim, H. K., Missiakas, D. M., & Schneewind, O. (2019) · Nature · doi:10.1038/s41586-019-1570-z · Cited by 80
Yuan, X., Nie, W., He, Z., Yang, H. J., Shao, B., Ma, X., Zhang, X., Bi, Z., Sun, L., Liang, X., et al. (2020) · Theranostics · doi:10.7150/thno.34065 · Cited by 82
Brock, R. M., Beitel-White, N., Davalos, R. V., & Allen, I. C. (2020) · Frontiers in Oncology · doi:10.3389/fonc.2020.01235 · Cited by 88
Mitochondrial Dysfunction in the Pathogenesis of Preeclampsia
Hu, X., & Zhang, L. (2022) · Current Hypertension Reports · doi:10.1007/s11906-022-01184-7 · Cited by 86
mTOR signaling networks: mechanistic insights and translational frontiers in disease therapeutics
Zhang, H., Xiao, X., Pan, Z., & Dokudovskaya, S. (2025) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02493-4 · Cited by 94
Sepsis: From Pathophysiology to Individualized Patient Care
László, I., Trásy, D., Molnár, Z., & Fazakas, J. (2015) · Journal of Immunology Research · doi:10.1155/2015/510436 · Cited by 92
Thundyil, J., & Lim, K. (2014) · Ageing Research Reviews · doi:10.1016/j.arr.2014.11.003 · Cited by 85
Valcarcel‐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
Aranda, F., Vacchelli, E., Obrist, F., Eggermont, A. M. M., Galon, J., Sautès‐Fridman, C., Cremer, I., ter Meulen, J. H., Zitvogel, L., Kroemer, G., et al. (2014) · OncoImmunology · doi:10.4161/onci.29179 · Cited by 85
Early and Transient Release of Leukocyte Pentraxin 3 during Acute Myocardial Infarction
Maugeri, N., Rovere, P. Q., Slavich, M., Coppi, G., Doni, A., Bottazzi, B., Garlanda, C., Cianflone, D., Maseri, A., Mantovani, A., et al. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1100261 · Cited by 84
Hazeldine, J., Hampson, P., Opoku, F., Foster, M., & Lord, J. M. (2015) · Injury · doi:10.1016/j.injury.2015.03.028 · Cited by 86
Glaucoma and neuroinflammation: An overview
Quaranta, L., Bruttini, C., Micheletti, E., Konstas, A. G. P., Michelessi, M., Oddone, F., Katsanos, A., Sbardella, D., Angelis, G. D., & Riva, I. (2021) · Survey of Ophthalmology · doi:10.1016/j.survophthal.2021.02.003 · Cited by 84
Neutrophils and COVID-19: Active Participants and Rational Therapeutic Targets
Hazeldine, J., & Lord, J. M. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.680134 · Cited by 86
Mitochondria and ischemia reperfusion injury
Panconesi, R., Widmer, J. D., Carvalho, M. F., Eden, J., Dondossola, D. E., Dutkowski, P., & Schlegel, A. A. (2022) · Current Opinion in Organ Transplantation · doi:10.1097/mot.0000000000001015 · Cited by 81
Persistent inflammation in HIV infection: Established concepts, new perspectives
Nasi, M., Pinti, M., Mussini, C., & Cossarizza, A. (2014) · Immunology Letters · doi:10.1016/j.imlet.2014.01.008 · Cited by 84
Naumann, D. N., Hazeldine, J., Midwinter, M. J., Hutchings, S., & Harrison, P. (2017) · The Journal of Trauma: Injury, Infection, and Critical Care · doi:10.1097/ta.0000000000001695 · Cited by 81
Koenig, A., & Buskiewicz, I. A. (2022) · Antioxidants and Redox Signaling · doi:10.1089/ars.2021.0073 · Cited by 78
Wilkins, H., Carl, S. M., Weber, S. G., Ramanujan, S., Festoff, B. W., Linseman, D. A., & Swerdlow, R. H. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-142334 · Cited by 83
Factors Influencing RBC Alloimmunization: Lessons Learned from Murine Models
Ryder, A. B., Zimring, J. C., & Hendrickson, J. E. (2014) · Transfusion Medicine and Hemotherapy · doi:10.1159/000368995 · Cited by 80
Kuck, J. L., Obiako, B. O., Gorodnya, O. M., Pastukh, V. M., Kua, J., Simmons, J. D., & Gillespie, M. N. (2015) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00015.2015 · Cited by 80
Using an agent-based model to analyze the dynamic communication network of the immune response
Folcik, V. A., Broderick, G., Mohan, S., Block, B., Ekbote, C., Doolittle, J., Khoury, M., Davis, L., & Marsh, C. B. (2011) · Theoretical Biology and Medical Modelling · doi:10.1186/1742-4682-8-1 · Cited by 81
Extracellular Ribonucleic Acids (RNA) Enter the Stage in Cardiovascular Disease
Zernecke, A., & Preissner, K. T. (2016) · Circulation Research · doi:10.1161/circresaha.115.307961 · Cited by 80
Urinary Mitochondrial DNA Copy Number Identifies Chronic Renal Injury in Hypertensive Patients
Eirin, A., Saad, A., Tang, H. J., Herrmann, S. M., Woollard, J. R., Lerman, A., Textor, S. C., & Lerman, L. O. (2016) · Hypertension · doi:10.1161/hypertensionaha.116.07849 · Cited by 81
Proteomics characterization of mitochondrial‐derived vesicles under oxidative stress
Vasam, G., Nadeau, R., Cadete, V. J. J., Lavallée‐Adam, M., Menzies, K. J., & Burelle, Y. (2021) · The FASEB Journal · doi:10.1096/fj.202002151r · Cited by 87
Host Response to Biomaterials for Cartilage Tissue Engineering: Key to Remodeling
Fu, W. E., Liu, S., Chen, M., Tian, G., Zha, K., Yang, Z., Jiang, S., Li, M., Sui, X., Chen, Z., et al. (2021) · Frontiers in Bioengineering and Biotechnology · doi:10.3389/fbioe.2021.664592 · Cited by 78
Xie, Q., Zeng, J., Zheng, Y., Li, T., Ren, J., Chen, K., Zhang, Q., Xie, R., Xu, F., & Zhu, J. (2021) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2021/1006636 · Cited by 80
Self-citationSong, Z., Xia, Y., Shi, L., Zha, H., Huang, J., Xiang, X., Li, H., Huang, H., Yue, R., Wang, H., et al. (2024) · Cellular & Molecular Biology Letters · doi:10.1186/s11658-024-00553-1 · Cited by 88
“Detection of circulating free mtDNA has even been considered as a potential biomarker for assessing tissue damage [48] .”
BackgroundCardioprotective potential of annexin-A1 mimetics in myocardial infarction
Qin, C. X., Yang, Y. H., May, L. T., Gao, X., Stewart, A. G., Tu, Y., Woodman, O. L., & Ritchie, R. H. (2014) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2014.11.012 · Cited by 79
Lee, Y.-L., King, M. B., Gonzalez, R. P., Brevard, S. B., Frotan, M. A., Gillespie, M. N., & Simmons, J. D. (2014) · Journal of Surgical Research · doi:10.1016/j.jss.2014.06.003 · Cited by 78
Bouhamida, E., Morciano, G., Perrone, M., Kahsay, A. E., Della Sala, M., Wieckowski, M. R., Fiorica, F., Pinton, P., Giorgi, C., & Patergnani, S. (2022) · Biology · doi:10.3390/biology11020300 · Cited by 87
Herbal Medicines for Ischemic Stroke: Combating Inflammation as Therapeutic Targets
Gu, Y., Chen, J., & Shen, J. (2014) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-014-9525-5 · Cited by 78
Niethammer, P. (2016) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2016.05.001 · Cited by 78
Yarbro, J. R., Emmons, R. S., & Pence, B. D. (2020) · Immunometabolism · doi:10.20900/immunometab20200026 · Cited by 83
Aging: All roads lead to mitochondria
Son, J. M., & Lee, C. D. (2021) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2021.02.006 · Cited by 86
Saada, J. I., McAuley, R. J., Marcatti, M., Tang, T. Z., Motamedi, M., & Szczęsny, B. (2021) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2021.101523 · Cited by 77
Pro-Inflammatory Signalling PRRopels Cisplatin-Induced Toxicity
Domingo, I. K., Latif, A., & Bhavsar, A. P. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23137227 · Cited by 83
“TLR9, another TLR PRR, is canonically geared towards the recognition of DNA structures associated with pathogens (unmethylated CpG-DNA motifs), but it has also been shown to recognise DNA-related DAMPs and bacterial by-products and components [42,94].”
BackgroundRedox signalling and mitochondrial stress responses; lessons from inborn errors of metabolism
Olsen, R. K. J., Cornelius, N., & Gregersen, N. (2015) · Journal of Inherited Metabolic Disease · doi:10.1007/s10545-015-9861-5 · Cited by 83
MGN1703, an immunomodulator and toll-like receptor 9 (TLR-9) agonist: From bench to bedside
Wittig, B., Schmidt, M., Scheithauer, W., & Schmoll, H. (2014) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2014.12.002 · Cited by 78
Preeclampsia and health risks later in life: an immunological link
Cheng, S., & Sharma, S. (2016) · Seminars in Immunopathology · doi:10.1007/s00281-016-0579-8 · Cited by 78
Zhang, L., Deng, S., Zhao, S., Ai, Y., Zhang, L., Pan, P., Su, X., Tan, H., & Wu, D. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17091425 · Cited by 78
The impact of sterile inflammation in acute liver injury
Woolbright, B. L. (2017) · Journal of Clinical and Translational Research · doi:10.18053/jctres.03.2017s1.003 · Cited by 79
DAMPs, PAMPs, and the Origins of SIRS in Bacterial Sepsis
Gentile, L. F., & Moldawer, L. L. (2012) · Shock · doi:10.1097/shk.0b013e318277109c · Cited by 78
Szczęsny, B., Brunyánszki, A., Ahmad, A., Oláh, G., Porter, C. C., Toliver-Kinsky, T. E., Sidossis, L. S., Herndon, D. N., & Szabó, C. (2015) · PLoS ONE · doi:10.1371/journal.pone.0143730 · Cited by 77
Scozzi, D., Ibrahim, M., Liao, F., Lin, X., Hsiao, H.-M., Hachem, R. R., Tague, L. K., Rícci, A., Kulkarni, H. S., Huang, H. J., et al. (2018) · American Journal of Transplantation · doi:10.1111/ajt.15232 · Cited by 78
Filep, J. G., & Ariel, A. (2020) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00181.2020 · Cited by 79
Expanding and validating the biomarkers for mitochondrial diseases
Maresca, A., Dotto, V. D., Romagnoli, M., Morgia, C. L., Vito, L. D., Capristo, M., Valentino, M. L., Carelli, V., & the ER-MITO Study Group (2020) · Journal of Molecular Medicine · doi:10.1007/s00109-020-01967-y · Cited by 77
From Mitochondria to Atherosclerosis: The Inflammation Path
Suarez-Rivero, J. M., Pastor‐Maldonado, C. J., Povea-Cabello, S., Álvarez-Córdoba, M., Villalón-García, I., Talaverón-Rey, M., Suárez-Carrillo, A., Munuera-Cabeza, M., & Sánchez-Alcázar, J. A. (2021) · Biomedicines · doi:10.3390/biomedicines9030258 · Cited by 78
Zhang, Y., Chu, J. M. T., & Wong, G. T. C. (2022) · Biomolecules · doi:10.3390/biom12040597 · Cited by 81
Mitochondrial-Derived Vesicles: The Good, the Bad, and the Ugly
Picca, A., Guerra, F., Calvani, R., Coelho‐Júnior, H. J., Landi, F., Bucci, C., & Marzetti, E. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241813835 · Cited by 81
“Indeed, mitochondrial DAMPs can guide the migration and degranulation of neutrophils at the site of injury, thereby further promoting cellular damage and local inflammation [9,96].”
BackgroundInfluentialNeutrophils come of age in chronic inflammation
Caielli, S., Banchereau, J., & Pascual, V. (2012) · Current Opinion in Immunology · doi:10.1016/j.coi.2012.09.008 · Cited by 79
Unuma, K., Aki, T., Funakoshi, T., Hashimoto, K., & Uemura, K. (2015) · Autophagy · doi:10.1080/15548627.2015.1063765 · Cited by 76
Carchman, E. H., Whelan, S., Loughran, P., Mollen, K. P., Stratamirovic, S., Shiva, S., Rosengart, M. R., & Zuckerbraun, B. S. (2013) · The FASEB Journal · doi:10.1096/fj.13-229476 · Cited by 77
Expression of Toll-like Receptors and Their Signaling Pathways in Rheumatoid Synovitis
Tamaki, Y., Takakubo, Y., Hirayama, T., Konttinen, Y. T., Goodman, S. B., Yamakawa, M., & Takagi, M. (2011) · The Journal of Rheumatology · doi:10.3899/jrheum.100732 · Cited by 82
Abboud, A., Namas, R. A., Ramadan, M., Mi, Q., Almahmoud, K., Abdul-Malak, O. M., Azhar, N., Zaaqoq, A. M., Namas, R. A., Barclay, D. A., et al. (2016) · Critical Care Medicine · doi:10.1097/ccm.0000000000001951 · Cited by 75
Pathogen- and Danger-Associated Molecular Patterns and the Cytokine Response in Sepsis
Rajaee, A., Barnett, R. L., & Cheadle, W. G. (2018) · Surgical Infections · doi:10.1089/sur.2017.264 · Cited by 81
Macrophages play an essential role in trauma-induced sterile inflammation and tissue repair
Peiseler, M., & Kubes, P. (2018) · European Journal of Trauma and Emergency Surgery · doi:10.1007/s00068-018-0956-1 · Cited by 79
Role of Hemichannels in CNS Inflammation and the Inflammasome Pathway
Kim, Y., Davidson, J. O., Gunn, K. C., Phillips, A. R. J., Green, C. R., & Gunn, A. J. (2015) · Advances in protein chemistry and structural biology · doi:10.1016/bs.apcsb.2015.12.001 · Cited by 76
Mitochondria: multifaceted regulators of aging
Son, J. M., & Lee, C. D. (2019) · BMB Reports · doi:10.5483/bmbrep.2019.52.1.300 · Cited by 76
Hamfjord, J., Guren, T. K., Dajani, O. F., Johansen, J. S., Glimelius, B. L. G., Sørbye, H., Pfeiffer, P., Lingjærde, O. C., Tveit, K. M., Kure, E. H., et al. (2019) · Annals of Oncology · doi:10.1093/annonc/mdz139 · Cited by 76
Li, L., Bi, Z., Hu, Y., Sun, L., Song, Y., Chen, S., Mo, F., Yang, J., Wei, Y., & Wei, X. (2020) · Cell Biology and Toxicology · doi:10.1007/s10565-020-09526-4 · Cited by 79
Immunology of Giant Cell Arteritis
Weyand, C. M., & Goronzy, J. J. (2023) · Circulation Research · doi:10.1161/circresaha.122.322128 · Cited by 84
Yu, B., Jin, L., Yao, X., Zhang, Y., Zhang, G., Wang, F., Su, X., Fang, Q., Liang, X., Yang, Y. A., et al. (2023) · Theranostics · doi:10.7150/thno.84655 · Cited by 76
“Disruption of mitochondria not only compromises production of energy but also increases production of reactive oxygen species (ROS) and induces release of cytochrome (Cyt)-c and mitochondrial DNA (mtDNA), triggering cell apoptosis and inflammation (10-12).”
BackgroundDuregotti, E., Negro, S., Scorzeto, M., Zornetta, I., Dickinson, B. C., Chang, C. J., Montecucco, C., & Rigoni, M. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1417108112 · Cited by 76
Spontaneous Neutrophil Migration Patterns during Sepsis after Major Burns
Jones, C. N., Moore, M. E., Dimisko, L., Alexander, A., Ibrahim, A., Hassell, B. A., Warren, H. S., Tompkins, R. G., Fagan, S. P., & Irimia, D. (2014) · PLoS ONE · doi:10.1371/journal.pone.0114509 · Cited by 74
A Tissue-Specific Role for Nlrp3 in Tubular Epithelial Repair after Renal Ischemia/Reperfusion
Bakker, P. J., Butter, L. M., Claessen, N., Teske, G. J. D., Sutterwala, F. S., Florquin, S., & Leemans, J. C. (2014) · American Journal Of Pathology · doi:10.1016/j.ajpath.2014.04.005 · Cited by 76
Tsutsui, H., Imamura, M., Fujimoto, J., & Nakanishi, K. (2010) · Gastroenterology Research and Practice · doi:10.1155/2010/641865 · Cited by 76
Formylpeptide Receptors Mediate Rapid Neutrophil Mobilization to Accelerate Wound Healing
Liu, M., Chen, K., Yoshimura, T., Liu, Y., Gong, W., Le, Y., Gao, J., Zhao, J., Wang, J. M., & Wang, A. (2014) · PLoS ONE · doi:10.1371/journal.pone.0090613 · Cited by 76
The Evolving Science of Trauma Resuscitation
Harris, T., Davenport, R. A., Mak, M., & Brohi, K. (2017) · Emergency Medicine Clinics of North America · doi:10.1016/j.emc.2017.08.009 · Cited by 76
Self-citationClark, I. A., Atwood, C., Bowen, R. L., Paz-Filho, G., & Vissel, B. (2012) · Pharmacological Reviews · doi:10.1124/pr.112.005850 · Cited by 76
Hu, Q., Wood, C. R., Cimen, S., Venkatachalam, A. B., & Alwayn, I. P. J. (2015) · PLOS ONE · doi:10.1371/journal.pone.0140105 · Cited by 75
Reactive Fibrosis Precedes Doxorubicin-Induced Heart Failure Through Sterile Inflammation
Tanaka, R., Umemura, M., Narikawa, M., Hikichi, M., Osaw, K., Fujita, T., Yokoyama, U., Ishigami, T., Tamura, K., & Ishikawa, Y. (2020) · ESC Heart Failure · doi:10.1002/ehf2.12616 · Cited by 75
Mitochondrial control of innate immune responses
Chen, S., Liao, Z., & Xu, P. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1166214 · Cited by 87
Infection, Inflammation, and Immunity in Sepsis
Das, U. N. (2023) · Biomolecules · doi:10.3390/biom13091332 · Cited by 75
“In addition, circulating mtDNA can activate Toll-like receptors (especially TLR9) and inflammasomes, contributing to sepsis [34,35].”
BackgroundShi, L., Zha, H., Zhou, P., Wang, J., Xia, Y., Li, H., Huang, H., Yue, R., Song, Z., & Zhu, J. (2023) · Cell Death and Disease · doi:10.1038/s41419-023-06247-4 · Cited by 79
“Detection of circulating free mtDNA is even considered a potential biomarker for assessing tissue damage [37].”
Heterogeneity in fibroblast proliferation and survival in idiopathic pulmonary fibrosis
Habiel, D. M., & Hogaboam, C. M. (2014) · Frontiers in Pharmacology · doi:10.3389/fphar.2014.00002 · Cited by 75
Molecular determinants of sterile inflammation
Kono, H., Onda, A., & Yanagida, T. (2014) · Current Opinion in Immunology · doi:10.1016/j.coi.2013.12.004 · Cited by 77
Cholesterol-Induced Membrane Microvesicles As Novel Carriers of Damage–Associated Molecular Patterns
Liu, M., Scalia, R. G., Mehta, J. L., & Williams, K. J. (2012) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.112.255471 · Cited by 75
Schiller, M. R., Parčina, M., Heyder, P., Foermer, S., Ostrop, J., Leo, A., Heeg, K. M., i, M. H., Lorenz, H., & Bekeredjian‐Ding, I. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1100631 · Cited by 76
Mitochondrial DNA and Toll-Like Receptor-9 Are Associated With Mortality in Critically Ill Patients
Krychtiuk, K. A., Ruhittel, S., Hohensinner, P. J., Koller, L., Kaun, C., Lenz, M. W., Bauer, B., Wutzlhofer, L. M., Draxler, D. F., Maurer, G., et al. (2015) · Critical Care Medicine · doi:10.1097/ccm.0000000000001311 · Cited by 75
Kapnick, S. M., Pacheco, S. E., & McGuire, P. J. (2017) · Metabolism · doi:10.1016/j.metabol.2017.11.010 · Cited by 76
Low-dose cadmium disrupts mitochondrial citric acid cycle and lipid metabolism in mouse lung
Hu, X. Y., Chandler, J. D., Park, S., Liu, K., Fernandes, J., Orr, M. C., Smith, M. R., Ma, C., Kang, S., Uppal, K., et al. (2018) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.12.005 · Cited by 75
Becker, Y., Loignon, R.-C., Julien, A.-S., Marcoux, G., Allaeys, I., Lévesque, T., Rollet-Labelle, E., Benk-Fortin, H., Cloutier, N., Melki, I., et al. (2019) · Scientific Reports · doi:10.1038/s41598-019-40900-3 · Cited by 75
Bakkour, S., Acker, J. P., Chafets, D. M., Inglis, H. C., Norris, P. J., Lee, T., & Busch, M. P. (2016) · Vox Sanguinis · doi:10.1111/vox.12390 · Cited by 74
Biomaterials for revascularization and immunomodulation after spinal cord injury
Haggerty, A. E., Maldonado, I. C., & Oudega, M. (2018) · Biomedical Materials · doi:10.1088/1748-605x/aaa9d8 · Cited by 74
The role of mitophagy in pulmonary sepsis
Mohsin, M., Tabassum, G., Ahmad, S., Ali, S., & Syed, M. A. (2021) · Mitochondrion · doi:10.1016/j.mito.2021.04.009 · Cited by 76
Pázmándi, K., Agod, Z., Kumar, B. V., Szabó, A., Fekete, T., Sógor, V., Veres, Á. N., Boldogh, I. R., Rajnavölgyi, É., Lányi, Á., et al. (2014) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2014.09.028 · Cited by 78
Dear, J. W., Simpson, K. J., Nicolai, M. P. J., Catterson, J. H., Street, J. M., Huizinga, T., Craig, D. G. N., Dhaliwal, K., Webb, S., Bateman, D. N., et al. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1100165 · Cited by 73
Neutrophil heterogeneity and its role in infectious complications after severe trauma
Hesselink, L., Spijkerman, R., van Wessem, K. J. P., Koenderman, L., Leenen, L. P. H., Huber-Lang, M. S., & Hietbrink, F. (2019) · World Journal of Emergency Surgery · doi:10.1186/s13017-019-0244-3 · Cited by 78
Meduri, G. U., & Chrousos, G. P. (2020) · Frontiers in Endocrinology · doi:10.3389/fendo.2020.00161 · Cited by 80
Barron, A., McCarthy, C., & O’Keeffe, G. W. (2021) · Molecular Neurobiology · doi:10.1007/s12035-021-02290-4 · Cited by 73
Metadata
- Authors
- Zhang, Q., Raoof, M., Chen, Y., Sumi, Y., Sursal, T., Junger, W., Brohi, K., Itagaki, K., & Hauser, C. J.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Queen Mary University of London (GB)
- Corresponding author
- Hauser, Carl J.
- ORCID
- Venue
- Nature
- Published
- 2010-03
- Volume
- 464
- Issue
- 7285
- Pages
- 104-107
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC2843437
- OpenAlex
- W2134219545
- Cited by
- 3,812
- References
- 34
- Citations by year
- 2026: 253 · 2025: 254 · 2024: 268 · 2023: 266 · 2022: 267 · 2021: 294 · 2020: 275 · 2019: 243 · 2018: 246 · 2017: 252 · 2016: 248 · 2015: 230 · 2014: 196 · 2013: 176 · 2012: 148
- FWCI
- 70.40
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- U.S. Department of Defense
- National Institute of General Medical Sciences (R01GM051477, R01GM059179)
- Congressionally Directed Medical Research Programs
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Sepsis Diagnosis and Treatment
- Keywords
- mitochondrial DAMPs, mitochondrial damage-associated molecular patterns, mitochondrial DNA, formyl peptides, FPR1, TLR9, neutrophils, systemic inflammatory response syndrome, trauma (physical injury), innate immunity, neutrophil degranulation, MAPK signaling, target organ damage
- MeSH terms
- Animals, Cells, Cultured, DNA, Mitochondrial, Femur, Humans, Immunity, Innate, Liver, Male, Mitochondria, N-Formylmethionine Leucyl-Phenylalanine, Neutrophils, Phosphorylation, Wounds and Injuries, Rats, Sprague-Dawley, Muscle, Skeletal, Systemic Inflammatory Response Syndrome, Sepsis, CpG Islands, Calcium Signaling, Mitogen-Activated Protein Kinases, Receptors, Formyl Peptide, Fractures, Bone, Toll-Like Receptor 9, Rats, Acute Lung Injury
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
