The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Interferon-γ Signaling Inhibition Ameliorates Angiotensin II–Induced Cardiac Damage
Open accessAbstract
Angiotensin (Ang) II induces vascular injury in part by activating innate and adaptive immunity; however, the mechanisms are unclear. We investigated the role of interferon (IFN)-γ and interleukin (IL)-23 signaling. We infused Ang II into IFN-γ receptor (IFN-γR) knockout mice and wild-type controls, as well as into mice treated with neutralizing antibodies against IL-23 receptor and IL-17A. Ang II–treated IFN-γR knockout mice exhibited reduced cardiac hypertrophy, reduced cardiac macrophage and T-cell infiltration, less fibrosis, and less arrhythmogenic electric remodeling independent of blood pressure changes. In contrast, IL-23 receptor antibody treatment did not reduce cardiac hypertrophy, fibrosis, or electric remodeling despite mildly reduced inflammation. IL-17A antibody treatment behaved similarly. In the kidney, IFN-γR deficiency reduced inflammation and tubulointerstitial damage and improved glomerular filtration rate. Nonetheless, albuminuria was increased compared with Ang II–treated wild-type controls. The glomeruli of Ang II–treated IFN-γR knockout mice exhibited fewer podocytes, less nephrin and synaptopodin staining, and impaired podocyte autophagy. Thus, IFN-γ blockade, but not IL-23 receptor antibody treatment, protects from Ang II–induced cardiac damage and electric remodeling. In the kidney, IFN-γ signaling acts in a cell type–specific manner. Glomerular filtration rate is preserved in the absence of the IFN-γR, whereas podocytes may require the IFN-γR in the presence of Ang II for normal integrity and function.
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Brenner, B. M., Cooper, M. E., de Zeeuw, D., Keane, W. F., Mitch, W. E., Parving, H.-H., Remuzzi, G., Snapinn, S. M., Zhang, Z., & Shahinfar, S. (2001) · New England Journal of Medicine · doi:10.1056/nejmoa011161 · Cited by 7,493
IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
Langrish, C. L., Chen, Y., Blumenschein, W. M., Mattson, J., Basham, B., Sedgwick, J. D., McClanahan, T., Kastelein, R. A., & Cua, D. J. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20041257 · Cited by 4,099
Cua, D. J., Sherlock, J., Chen, Y., Murphy, C. A., Joyce, B., Seymour, B., Lucian, L., To, W., Kwan, S., Churakova, T., et al. (2003) · Nature · doi:10.1038/nature01355 · Cited by 2,906
Liang, S. C., Tan, X.-Y., Luxenberg, D. P., Karim, R., Dunussi-Joannopoulos, K., Collins, M., & Fouser, L. A. (2006) · The Journal of Experimental Medicine · doi:10.1084/jem.20061308 · Cited by 2,330
Fibrotic disease and the TH1/TH2 paradigm
Wynn, T. A. (2004) · Nature Reviews Immunology · doi:10.1038/nri1412 · Cited by 1,765
Role of the T cell in the genesis of angiotensin II–induced hypertension and vascular dysfunction
Guzik, T. J., Hoch, N. E., Brown, K. A., McCann, L. A., Rahman, A., Dikalov, S., Goronzy, J., Weyand, C., & Harrison, D. G. (2007) · The Journal of Experimental Medicine · doi:10.1084/jem.20070657 · Cited by 1,736
Generation of pathogenic TH17 cells in the absence of TGF-β signalling
Ghoreschi, K., Laurence, A., Yang, X.-P., Tato, C. M., McGeachy, M. J., Konkel, J. E., Ramos, H. L., Wei, L., Davidson, T. S., Bouladoux, N., et al. (2010) · Nature · doi:10.1038/nature09447 · Cited by 1,388
Hartleben, B., Gödel, M., Meyer-Schwesinger, C., Liu, S., Ulrich, T., Köbler, S., Wiech, T., Grahammer, F., Arnold, S. J., Lindenmeyer, M. T., et al. (2010) · Journal of Clinical Investigation · doi:10.1172/jci39492 · Cited by 721
Cited by
Cardiac Fibrosis: The Fibroblast Awakens
Travers, J. G., Kamal, F. A., Robbins, J., Yutzey, K. E., & Blaxall, B. C. (2016) · Circulation Research · doi:10.1161/circresaha.115.306565 · Cited by 1,596
Inflammation, Immunity, and Hypertensive End-Organ Damage
McMaster, W. G., Kirabo, A., Madhur, M. S., & Harrison, D. G. (2015) · Circulation Research · doi:10.1161/circresaha.116.303697 · Cited by 708
Perivascular adipose tissue inflammation in vascular disease
Nosalski, R., & Guzik, T. J. (2017) · British Journal of Pharmacology · doi:10.1111/bph.13705 · Cited by 398
Role of the Immune System in Hypertension
Rodriguez-Iturbe, B., Pons, H., & Johnson, R. J. (2017) · Physiological Reviews · doi:10.1152/physrev.00031.2016 · Cited by 391
Zhang, Z., Zhao, L., Zhou, X., Meng, X., & Zhou, X. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2022.1098725 · Cited by 382
Metadata
- Authors
- Markó, L., Kvakan, H., Park, J.-K., Qadri, F., Spallek, B., Binger, K. J., Bowman, E. P., Kleinewietfeld, M., Fokuhl, V., Dechend, R., & Müller, D. N.
- Venue
- Hypertension
- Published
- 2012-12
- Volume
- 60
- Issue
- 6
- Pages
- 1430-1436
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2129728198
- Cited by
- 184
- References
- 8
- FWCI
- 7.48
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Interferon-γ Signaling Inhibition Ameliorates Angiotensin II–Induced Cardiac Damage. https://app.cochat.ai/papers/10.1161/hypertensionaha.112.199265
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- Markó, L., Kvakan, H., Park, J.-K., Qadri, F., Spallek, B., Binger, K. J., Bowman, E. P., Kleinewietfeld, M., Fokuhl, V., Dechend, R., & Müller, D. N. (2012). Interferon-γ Signaling Inhibition Ameliorates Angiotensin II–Induced Cardiac Damage. Hypertension. https://doi.org/10.1161/hypertensionaha.112.199265
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