Interleukin-6 deficiency attenuates angiotensin II-induced cardiac pathogenesis with increased myocyte hypertrophy

Chen, Fan; Chen, Dandan; Zhang, Yubin; Jin, Liang; Zhang, Han; Wan, Miyang; Pan, Tianshu; Wang, Xiaochuan; Su, Yuheng; Xu, Yitao; Ye, Junmei

doi:10.1016/j.bbrc.2017.10.119

Cited by 23 publications

(16 citation statements)

References 22 publications

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“…This effect was linked with extensive heart fibrosis and hypertrophy of the left ventricle in a rat model 37 . Decreased inflammatory reaction and inhibition of heart fibrosis were reported in IL‐6 knockout mice treated with angiotensin‐II 38 . In addition, González et al report that lack of IL‐6 protects the heart from inflammation, fibrosis and dysfunction; 8 the cytokine suppresses hypertrophy of the left ventricle, protects cardiac myocytes from apoptosis in pressure‐overloaded hearts and attenuates the area of heart injury 39 .…”

Section: Discussionmentioning

confidence: 92%

The stiffness‐controlled release of interleukin‐6 by cardiac fibroblasts is dependent on integrin α2β1

Gałdyszyńska

Bobrowska

Lekka

et al. 2020

J Cellular Molecular Medi

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Section: Discussionmentioning

confidence: 92%

The stiffness‐controlled release of interleukin‐6 by cardiac fibroblasts is dependent on integrin α2β1

Gałdyszyńska

Bobrowska

Lekka

et al. 2020

J Cellular Molecular Medi

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“…The specific role of IL‐6/gp130 signalling in HHD still needs more studies to elucidate. In addition to the pro‐hypertrophic role of IL‐6 in rats, IL‐6 deficiency was found to attenuate AngⅡ induced cardiac pathology and excessive activation of gp130 induces myocardial hypertrophy in mice . In contrary to the notion that IL‐6 might be pro‐hypertrophic and fibrotic, Kaminski et al and Lai et al considered IL‐6 as non‐essential in cardiac hypertrophy using IL‐6 knockout mice.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Interleukin‐6/glycoprotein 130 signalling by Bazedoxifene ameliorates cardiac remodelling in pressure overload mice

Shi

Liu

et al. 2020

J Cellular Molecular Medi

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The role of IL-6 signalling in hypertensive heart disease and its sequelae is controversial. Our group demonstrated that Bazedoxifene suppressed IL-6/gp130 signalling in cancer cells but its effect on myocardial pathology induced by pressure overload is still unknown. We explored whether Bazedoxifene could confer benefits in wildtype C57BL/6J mice suffering from transverse aortic constriction (TAC) and the potential mechanisms in H9c2 myoblasts. Mice were randomized into three groups (Sham, TAC, TAC+Bazedoxifene, n = 10). Morphological and histological observations suggested TAC aggravated myocardial remodelling while long-term intake of Bazedoxifene (5 mg/kg, intragastric) attenuated pressure overload-induced pathology. Echocardiographic results indicated Bazedoxifene rescued cardiac function in part. We found Bazedoxifene decreased the mRNA expression of IL-6, MMP2, Col1A1, Col3A1 and periostin in murine hearts after 8-week surgery. By Western blot detection, we found Bazedoxifene exhibited an inhibition of STAT3 activation in mice three hours and 8 weeks after TAC. Acute TAC stress (3 hours) led to downregulated ratio of LC3-Ⅱ/LC3-Ⅰ, while in mice after long-term (8 weeks) TAC this ratio becomes higher than that in Sham mice. Bazedoxifene inverted the autophagic alteration induced by TAC at both two time-points. In H9c2 myoblasts, Bazedoxifene suppressed the IL-6-induced STAT3 activation. Moreover, IL-6 reduced the ratio of LC3-Ⅱ/LC3-Ⅰ, promoted P62 expression but Bazedoxifene reversed both changes in | 4749 SHI et al.

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“…Given the current findings, IL-6 exerts anti-obesity effects in lipid metabolism. In contrast, another study suggested that a high-fat diet (HFD) caused more body-weight loss in Il6 À/À mice than in wild-type mice (Chen et al, 2017). Deficiency of IL-6 upregulates expression of cardiac fatty-acid transporters such as CD36 and the plasma membrane isoform of fatty-acid binding protein, suggesting that IL-6 may play a role in causing cardiac lipotoxicity (Coort et al, 2004;Luiken et al, 2001).…”

Section: Il-6 Receptor Signaling Pathwaymentioning

confidence: 99%

Targeting Interleukin-6 Signaling in Clinic

Tanaka²,

et al. 2019

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Interleukin-6 (IL-6) is a pleiotropic cytokine with roles in immunity, tissue regeneration, and metabolism. Rapid production of IL-6 contributes to host defense during infection and tissue injury, but excessive synthesis of IL-6 and dysregulation of IL-6 receptor signaling is involved in disease pathology. Therapeutic agents targeting the IL-6 axis are effective in rheumatoid arthritis, and applications are being extended to other settings of acute and chronic inflammation. Recent studies reveal that selective blockade of different modes of IL-6 receptor signaling has different outcomes on disease pathology, suggesting novel strategies for therapeutic intervention. However, some inflammatory diseases do not seem to respond to IL-6 blockade.Here, we review the current state of IL-6-targeting approaches in the clinic and discuss how to apply the growing understanding of the immunobiology of IL-6 to clinical decisions.

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Interleukin-6 deficiency attenuates angiotensin II-induced cardiac pathogenesis with increased myocyte hypertrophy

Cited by 23 publications

References 22 publications

The stiffness‐controlled release of interleukin‐6 by cardiac fibroblasts is dependent on integrin α2β1

The stiffness‐controlled release of interleukin‐6 by cardiac fibroblasts is dependent on integrin α2β1

Inhibition of Interleukin‐6/glycoprotein 130 signalling by Bazedoxifene ameliorates cardiac remodelling in pressure overload mice

Targeting Interleukin-6 Signaling in Clinic

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