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Cited by 474

The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

The AIM2 inflammasome exacerbates atherosclerosis in clonal haematopoiesis

Fidler, Trevor P., Xue, Chenyi, Yalcinkaya, Mustafa, Hardaway, Brian, Abramowicz, Sandra, Xiao, Tong, Liu, Wenli, Thomas, David G., Hajebrahimi, Mohammad Ali, Pircher, Joachim, Silvestre-Roig, Carlos, Kotini, Andriana G., Luchsinger, Larry L., Wei, Ying, Westerterp, Marit, Snoeck, Hans-Willem, Papapetrou, Eirini P., Schulz, Christian, Massberg, Steffen, Soehnlein, Oliver, Ebert, Benjamin, Levine, Ross L., Reilly, Muredach P., Libby, Peter, Wang, Nan, Tall, Alan R.·2021·Nature
DOI 10.1038/s41586-021-03341-5PMC PMC8038646
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Research works printed but not linked: 32

  1. Benjamin, E. J. et al. Heart disease and stroke statistics—2019 update: a report from the American Heart Association. Circulation 139, e56–e528 (2019). · DOI · Paper page
  2. Ridker, P. M. et al. Antiinflammatory therapy with Canakinumab for atherosclerotic disease. N. Engl. J. Med. 377, 1119–1131 (2017). · DOI · Paper page
  3. Landolfi, R. et al. Efficacy and safety of low-dose aspirin in polycythemia vera. N. Engl. J. Med. 350, 114–124 (2004). · DOI
  4. Cordua, S. et al. Prevalence and phenotypes of JAK2 V617F and calreticulin mutations in a Danish general population. Blood 134, 469–479 (2019). · DOI
  5. Wang, W. et al. Macrophage inflammation, erythrophagocytosis, and accelerated atherosclerosis in Jak2V617F mice. Circ. Res. 123, e35–e47 (2018). · DOI · Paper page
  6. Mullally, A. et al. Physiological Jak2V617F expression causes a lethal myeloproliferative neoplasm with differential effects on hematopoietic stem and progenitor cells. Cancer Cell 17, 584–596 (2010). · DOI
  7. Robbins, C. S. et al. Local proliferation dominates lesional macrophage accumulation in atherosclerosis. Nat. Med. 19, 1166–1172 (2013). · DOI · Paper page
  8. Edelmann, B. et al. JAK2-V617F promotes venous thrombosis through β1/β2 integrin activation. J. Clin. Invest. 128, 4359–4371 (2018). · DOI · Paper page
  9. Snippert, H. J. et al. Intestinal crypt homeostasis results from neutral competition between symmetrically dividing Lgr5 stem cells. Cell 143, 134–144 (2010). · DOI · Paper page
  10. Liu, D. J. et al. Exome-wide association study of plasma lipids in >300,000 individuals. Nat. Genet. 49, 1758–1766 (2017). · DOI · Paper page
  11. Hansson, G. K., Libby, P. & Tabas, I. Inflammation and plaque vulnerability. J. Intern. Med. 278, 483–493 (2015). · DOI
  12. Anderson, K. L. et al. PU.1 and the granulocyte- and macrophage colony-stimulating factor receptors play distinct roles in late-stage myeloid cell differentiation. Blood 94, 2310–2318 (1999). · DOI
  13. Rajavashisth, T. et al. Heterozygous osteopetrotic (op) mutation reduces atherosclerosis in LDL receptor-deficient mice. J. Clin. Invest. 101, 2702–2710 (1998). · DOI
  14. Shimada, K. et al. Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis. Immunity 36, 401–414 (2012). · DOI · Paper page
  15. Hu, B. et al. The DNA-sensing AIM2 inflammasome controls radiation-induced cell death and tissue injury. Science 354, 765–768 (2016). · DOI
  16. Schwartz, D. M. et al. JAK inhibition as a therapeutic strategy for immune and inflammatory diseases. Nat. Rev. Drug Discov. 16, 843–862 (2017). · DOI · Paper page
  17. Katherine, L. et al. Cloning a novel member of the human interferon-inducible gene family associated with control of tumorigenicity in a model of human melanoma. Oncogene 15, 453–457 (1997). · DOI
  18. Paulin, N. et al. Double-strand DNA sensing Aim2 inflammasome regulates atherosclerotic plaque vulnerability. Circulation 138, 321–323 (2018). · DOI
  19. Zernecke, A. et al. Meta-analysis of leukocyte diversity in atherosclerotic mouse aortas. Circ. Res. 127, 402–426 (2020). · DOI
  20. Mesa, R. A. et al. Effects of ruxolitinib treatment on metabolic and nutritional parameters in patients with myelofibrosis from COMFORT-I. Clin. Lymphoma Myeloma Leuk. 15, 214–221.e1 (2015). · DOI
  21. Rao, T. N. et al. JAK2-mutant hematopoietic cells display metabolic alterations that can be targeted to treat myeloproliferative neoplasms. Blood 134, 1832–1846 (2019). · DOI
  22. Choudhury, R. P. et al. Arterial effects of Canakinumab in patients with atherosclerosis and type 2 diabetes or glucose intolerance. J. Am. Coll. Cardiol. 68, 1769–1780 (2016). · DOI
  23. Bick, A. G. et al. Genetic interleukin 6 signaling deficiency attenuates cardiovascular risk in clonal hematopoiesis. Circulation 141, 124–131 (2020). · DOI · Paper page
  24. Vromman, A. et al. Stage-dependent differential effects of interleukin-1 isoforms on experimental atherosclerosis. Eur. Heart J. 40, 2482–2491 (2019). · DOI
  25. Mullally, A. et al. Distinct roles for long-term hematopoietic stem cells and erythroid precursor cells in a murine model of Jak2V617F-mediated polycythemia vera. Blood 120, 166–172 (2012). · DOI
  26. Iacobucci, I. et al. Truncating erythropoietin receptor rearrangements in acute lymphoblastic leukemia. Cancer Cell 29, 186–200 (2016). · DOI
  27. Maude, S. L. et al. Efficacy of JAK/STAT pathway inhibition in murine xenograft models of early T-cell precursor (ETP) acute lymphoblastic leukemia. Blood 125, 1759–1767 (2015). · DOI
  28. Thomas, D. G. et al. LXR suppresses inflammatory gene expression and neutrophil migration through cis-repression and cholesterol efflux. Cell Rep. 25, 3774–3785.e4 (2018). · DOI
  29. Thomas, P. D. et al. PANTHER: a library of protein families and subfamilies indexed by function. Genome Res. 13, 2129–2141 (2003). · DOI
  30. Kotini, A. G. et al. Stage-specific human induced pluripotent stem cells map the progression of myeloid transformation to transplantable leukemia. Cell Stem Cell 20, 315–328.e7 (2017). · DOI
  31. Fidler, T. P. et al. Glucose metabolism is required for platelet hyperactivation in a murine model of type 1 diabetes. Diabetes 68, 932–938 (2019). · DOI
  32. Durinck, S., Spellman, P. T., Birney, E. & Huber, W. Mapping identifiers for the integration of genomic datasets with the R/Bioconductor package biomaRt. Nat. Protocols 4, 1184–1191 (2009). · DOI

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Metadata

Authors
Fidler, T. P., Xue, C., Yalcinkaya, M., Hardaway, B., Abramowicz, S., Xiao, T., Liu, W., Thomas, D. G., Hajebrahimi, M. A., Pircher, J., Silvestre-Roig, C., Kotini, A. G., Luchsinger, L. L., Wei, Y., Westerterp, M., Snoeck, H.-W., Papapetrou, E. P., Schulz, C., Massberg, S., Soehnlein, O., Ebert, B., Levine, R. L., Reilly, M. P., Libby, P., Wang, N., & Tall, A. R.
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
2021-03-17
Volume
592
Issue
7853
Pages
296-301
ISSN
  • 0028-0836
  • 1476-4687
DOI
10.1038/s41586-021-03341-5
PMC
PMC8038646
Cited by
474
References
11
Language
en
Update notices
correction (2026-05-14)
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CoChat. (2026). Citation check: The AIM2 inflammasome exacerbates atherosclerosis in clonal haematopoiesis. https://app.cochat.ai/papers/10.1038/s41586-021-03341-5
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Fidler, T. P., Xue, C., Yalcinkaya, M., Hardaway, B., Abramowicz, S., Xiao, T., Liu, W., Thomas, D. G., Hajebrahimi, M. A., Pircher, J., Silvestre-Roig, C., Kotini, A. G., Luchsinger, L. L., Wei, Y., Westerterp, M., Snoeck, H.-W., Papapetrou, E. P., Schulz, C., Massberg, S., . . . Tall, A. R. (2021). The AIM2 inflammasome exacerbates atherosclerosis in clonal haematopoiesis. Nature. https://doi.org/10.1038/s41586-021-03341-5