Effects of therapy using the Celacade system on structural and functional cardiac remodelling in rats following myocardial infarction

Zhang, Mei Luo; Mei, Jie; Archer, Lori Anne; Obayashi, Masanao; Diao, Ni; Stuyvers, Bruno D.; Keurs, H. E. D. J. Ter

doi:10.1016/s0828-282x(09)70510-0

Cited by 6 publications

(2 citation statements)

References 31 publications

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“…The treated sample is then administered back to animals/patients intramuscularly, at which point the apoptotic cells stimulate anti-inflammatory cytokines and suppress pro-inflammatory cytokines, thereby creating an anti-inflammatory effect. In rats, IMT by the celacade system does not attenuate cardiac dilation post MI, but reduces LV diastolic dysfunction and restores the positive inotropism of pacing post MI [279]. In a double-blinded, placebo-controlled study, patients with functional class II-IV heart failure were randomly assigned to receive IMT or placebo by intragluteal injection on days 1, 2, 14, and every 28 days thereafter.…”

Section: Treatment With Tnfa Antagonists In Patients With Heart Failurementioning

confidence: 99%

TNFα in myocardial ischemia/reperfusion, remodeling and heart failure

2010

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TNFα is crucially involved in the pathogenesis and progression of myocardial ischemia/reperfusion injury and heart failure. The formation and release of TNFα and its downstream signal transduction cascade following activation of its two receptor subtypes are characterized. Myocardial TNFα and TNF receptor activation have an ambivalent role in myocardial ischemia/reperfusion injury and protection from it. Excessive TNFα expression and subsequent cardiomyocyte TNF receptor type 1 stimulation induce contractile dysfunction, hypertrophy, fibrosis and cell death, while a lower TNFα concentration and subsequent cardiomyocyte TNF receptor type 2 stimulation are protective. Apart from its concentration and receptor subtype, the myocardial action of TNFα depends on the duration of its exposure and its localization. While detrimental during sustained ischemia, TNFα contributes to ischemic preconditioning protection, no matter whether it is the first, second or third window of protection, and both TNF receptors are involved in the protective signal transduction cascade. Finally, the available clinical attempts to antagonize TNFα in cardiovascular disease, notably heart failure, are critically discussed.

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Section: Treatment With Tnfa Antagonists In Patients With Heart Failurementioning

confidence: 99%

TNFα in myocardial ischemia/reperfusion, remodeling and heart failure

2010

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“…Transforming growth factor-b1 (TGF-b1) has been implicated as a major contributor to tissue fibrosis in various organ systems. Expression of TGF-b1 is increased in both infarcted and noninfarcted areas of the hearts after MI [4,5]. TGF-b1 stimulates CF proliferation and differentiation into myofibroblast [6].…”

Section: Introductionmentioning

confidence: 99%