Systemic inflammation and cell activation reflects morbidity in chronic heart failure

Dixon, Dani‐Louise; Griggs, Kim; Bersten, Andrew D.; Pasquale, Carmine G. De

doi:10.1016/j.cyto.2011.08.029

Cited by 55 publications

(42 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Concentrations of TGF-b1 were higher in patients with chronic HF compared to healthy matched controls, and correlated with NYHA class [52]. In patients with end-stage HF undergoing cardiac transplant, TGF-b1 bioactivity measured in cardiac tissue was substantially higher in diseased heart tissue compared to tissue samples of healthy donor hearts.…”

Section: Tgf-b1 and Hf And Prognosismentioning

confidence: 79%

Biomarkers of apoptosis, inflammation, and cardiac extracellular matrix remodelling in the prognosis of heart failure

Osmančík

Louckova

2017

Kardiol Pol

View full text Add to dashboard Cite

Section: Tgf-b1 and Hf And Prognosismentioning

confidence: 79%

Biomarkers of apoptosis, inflammation, and cardiac extracellular matrix remodelling in the prognosis of heart failure

Osmančík

Louckova

2017

Kardiol Pol

View full text Add to dashboard Cite

“…In this study, the intragraft examination revealed that SAHA SAHA inhibits allograft rejection X Zhang et al 395 upregulated the expressions of Foxp3 and CTLA-4, but downregulated CD11b and IL-17. As CD11b is associated with the activation of monocytes and neutrophilic granulocytes, 49 the downregulation of CD11b revealed an improvement on intragraft infiltration. As Th17 are not the only IL-17 producing cell, 50 we isolated CD4 1 T cells and confirmed the downregulation of IL-17 in CD4 1 T cell subset by FCM analysis in vitro.…”

Section: Discussionmentioning

confidence: 91%

SAHA, an HDAC inhibitor, synergizes with tacrolimus to prevent murine cardiac allograft rejection

et al. 2012

View full text Add to dashboard Cite

Suberoylanilide hydroxamic acid (SAHA), as a histone deacetylase (HDAC) inhibitor (HDACi), was recently found to exhibit an immunosuppressive effect. However, whether SAHA can synergize with calcineurin inhibitors (CNIs) to inhibit allograft rejection and its underlying mechanism remain elusive. In this study, we demonstrated the synergistic effects of SAHA and non-therapeutic dose of tacrolimus (FK506) in prolonging the allograft survival in a murine cardiac transplant model. Concomitant intragraft examination revealed that allografts from SAHA-treated recipients showed significantly lower levels of IL-17 expression, and no discernable difference for IL-17 expressions was detected between SAHA-and SAHA/FK506-treated allograft as compared with allografts from FK506-treated animals. In contrast, administration of FK506 significantly suppressed interferon (IFN)-c but increased IL-10 expression as compared with that of SAHA-treated animals, and this effect was independent of SAHA. Interestingly, SAHA synergizes with FK506 to promote Foxp3 and CTLA4 expression. In vitro, SAHA reduced the proportion of Th17 cells in isolated CD4 1 T-cell population and decreased expressions of IL-17A, IL-17F, STAT3 and RORct in these cells. Moreover, SAHA enhances suppressive function of regulatory T (Treg) cells by upregulating the expression of CTLA-4 without affecting T effector cell proliferation, and increased the proportion of Treg by selectively promoting apoptosis of T effector cells. Therefore, SAHA, a HDACi, may be a promising immunosuppressive agent with potential benefit in conjunction with CNI drugs.

show abstract

“…Accordingly, elevated blood monocyte counts in patients after MI negatively correlate with ejection fraction (39). Along these lines, humans and mice with heart failure also display a blood leukocytosis (3,40,41). In general, elevated white blood cell numbers are an independent risk factor for CAD (42)(43)(44) and more specifically, higher monocyte counts independently predict risk for atherosclerosis after adjustment for conventional risk factors (45)(46)(47)(48)(49).…”

Section: Monocytes/macrophages In the Post-mi Phasementioning

confidence: 93%

Monocytes and macrophages in cardiac injury and repair

Sager¹,

Kessler²,

Schunkert³

2017

J. Thorac. Dis.

View full text Add to dashboard Cite

Systemic inflammation and cell activation reflects morbidity in chronic heart failure

Cited by 55 publications

References 23 publications

Biomarkers of apoptosis, inflammation, and cardiac extracellular matrix remodelling in the prognosis of heart failure

Biomarkers of apoptosis, inflammation, and cardiac extracellular matrix remodelling in the prognosis of heart failure

SAHA, an HDAC inhibitor, synergizes with tacrolimus to prevent murine cardiac allograft rejection

Monocytes and macrophages in cardiac injury and repair

Contact Info

Product

Resources

About