Interferon-γ Signaling Inhibition Ameliorates Angiotensin II–Induced Cardiac Damage

Markó, Lajos; Kvakan, Heda; Park, Joon-Keun; Qadri, Fatimunnisa; Spallek, Bastian; Binger, Katrina J.; Bowman, Edward P.; Kleinewietfeld, Markus; Fokuhl, Verena; Dechend, Ralf; Müller, Dominik N.

doi:10.1161/hypertensionaha.112.199265

Cited by 147 publications

(123 citation statements)

References 29 publications

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“…We and others have shown that the NADPH oxidase is critical for many forms of hypertension. Importantly, O 2 ·-serves as a progenitor for many IFN-γ, which have also been implicated in hypertension (5,29,30). In keeping with a critical role of DCs in this disease, we also found that hypertension causes a striking alteration of DC gene expression and that these alterations were in large part mediated by ROS derived from the NOX2 containing NADPH oxidase and by isoketal formation.…”

Section: Discussionsupporting

confidence: 82%

DC isoketal-modified proteins activate T cells and promote hypertension

et al. 2014

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Section: Discussionsupporting

confidence: 82%

DC isoketal-modified proteins activate T cells and promote hypertension

et al. 2014

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“…IL-23 receptor antibody treatment or IL-17A antibody treatment of Ang II-infused mice showed no major effect on cardiac or renal injury. 45 It has to be kept in mind that antibody treatment never has an efficiency of 100%, whereas a genetic approach knocks down the gene and protein of interest to 0%. Dermal overexpression of IL-17A induces not only psoriasis-like lesions but also endothelial dysfunction, vascular oxidative stress, and arterial hypertension.…”

Section: T H 1 and T Hmentioning

confidence: 99%

Immune Mechanisms in Arterial Hypertension

Wenzel¹,

Turner²,

Krebs³

et al. 2016

Journal of the American Society of Nephrology

165

146

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Traditionally, arterial hypertension and subsequent end-organ damage have been attributed to hemodynamic factors, but increasing evidence indicates that inflammation also contributes to the deleterious consequences of this disease. The immune system has evolved to prevent invasion of foreign organisms and to promote tissue healing after injury. However, this beneficial activity comes at a cost of collateral damage when the immune system overreacts to internal injury, such as prehypertension. Renal inflammation results in injury and impaired urinary sodium excretion, and vascular inflammation leads to endothelial dysfunction, increased vascular resistance, and arterial remodeling and stiffening. Notably, modulation of the immune response can reduce the severity of BP elevation and hypertensive endorgan damage in several animal models. Indeed, recent studies have improved our understanding of how the immune response affects the pathogenesis of arterial hypertension, but the remarkable advances in basic immunology made during the last few years still await translation to the field of hypertension. This review briefly summarizes recent advances in immunity and hypertension as well as hypertensive end-organ damage.

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“…Marko et al (19) found that while IFN-γ receptor-deficient mice exhibited reduced cardiac hypertrophy and decreased renal inflammation and tubulointerstitial damage compared with WT mice when infused with Ang II, there was no change in BP. However, they used a slightly different mouse model and a very high dose of Ang II (approximately twice the dose that we used).…”

Section: Ifn-γ Promotes Ang Ii-dependent Hypertensionmentioning

confidence: 99%