A Single Intravenous sTNFR-Fc Administration at the Time of Reperfusion Limits Infarct Size—Implications in Reperfusion Strategies in Man

Toufektsian, Marie-Claire; Robbez-Masson, Vanessa; Sanou, Drissa; Jouan, Marie-Gabrielle; Ormezzano, Olivier; Leiris, Joël de; Boucher, François

doi:10.1007/s10557-008-6130-y

Cited by 12 publications

(5 citation statements)

References 28 publications

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“…Thus, they used a single intravenous injection of soluble TNF-α receptor at the time of reperfusion and they tried to find whether it could reduce the infract size and improve post-ischemic cardiac function in vivo in rats. They concluded that inhibition of increased TNF-α production by a single IV injection of sTNFR-Fc improved post-infract outcome in rats [25]. …”

Section: Inflammatory Markers and Atherosclerosis Progression – Link mentioning

confidence: 99%

Serotonin reuptake inhibitor antidepressants (SSRIs) against atherosclerosis

et al. 2011

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SummarySelective serotonin reuptake inhibitors (SSRIs) are a class of drug widely used for treatment of mood disorders, including depression and cardiovascular disease. A search for related articles in the PubMed database was attempted. It covered studies, reports, reviews and editorials of the last 5 years.Pro-inflammatory cytokines, such as TNF-α, IL-1 and IL-6, stimulate central serotonin (5-HT) neurotransmission and are over-expressed in depression, which has been linked with hypothalamic-pituitary-adrenal axis (HPA) hyperactivity. They have also been implicated in the pathogenesis and progression of other stress-induced disorders, like myocardial infarction (MI) and coronary heart disease (CHD), as they seem to modulate cardiovascular function by a variety of mechanisms. Biological mechanisms like these may explain the link between depression and CHD. There are a variety of environmental factors as well as genetic factors that might influence the pharmacogenetics of antidepressant drugs. New generation selective serotonin reuptake inhibitor antidepressants (SSRIs) causing a reduced cardiovascular morbidity and mortality may be related to serotonin platelet abnormalities in depressed patients that are effectively treated by SSRIs. SSRIs such as fluoxetine, paroxetine, sertraline and citalopram are not only considered to be free from the cardiotoxicity of their predecessors but also to function as safe and efficacious agents against depression, platelet activation, atherosclerosis and development and prognosis of coronary heart disease. However, there is a need for more studies in order to establish the exact biochemical mechanisms that are responsible for these diseases and the immunoregulatory effects of chronic use of SSRI medications.

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Section: Inflammatory Markers and Atherosclerosis Progression – Link mentioning

confidence: 99%

Serotonin reuptake inhibitor antidepressants (SSRIs) against atherosclerosis

et al. 2011

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“…TNF-α levels were found higher in patients suffering from heart failure [49]. In a variety of experimental MI models, the treatment with IL-1β [50], IL-6 [51] or TNF α [52]inhibiting agent showed positive effects on left LVEF and infarct size. Similarly, in our present study the involvement of proin ammatory cytokines decrease in SFN's cardioprotection was also demonstrated in vivo and in vitro.…”

Section: Discussionmentioning

confidence: 96%

Porous magnetic Silica nanoparticles loaded with sulforaphane mitigate myocardial infarction injury through upregulating HSP70

Zhang

Dong

et al. 2022

Preprint

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Myocardial infarction (MI) is a common cardiovascular disease that induces an extensive sterile inflammation in the early stage, but usually seriously endangers human health. The modulation of cardiac inflammation may improve the outcome of post MI. Unfortunately, due to therapeutic drugs’ side effects and the cardiac coronary artery occlusion, currently MI drugs always can hardly fulfill the myocardial ischemia environment and clinical requirements. Considering the myocardial protective effect and low toxicity of sulforaphane (SFN), SFN was adopted for the treatment of MI. However, it is still difficult for the targeted accumulation of SFN in the infarcted area. Herein, porous magnetic silica nanoparticles (PMSNs) were synthesized and loaded with sulforaphane (SFN) to improve the efficiency by targeted delivery to the infarcted area in MI mice. PMSNs loaded with SFN (PMSNs+SFN) decreased the pro-inflammatory cytokines, thus improving the cardiac functions and cell survival without any adverse effects. To further explore the mechanism by which SFN treated MI mice, oxygen and glucose deprivation (OGD) cells was established as a cellular model for the in vitro study of MI. Knockdown of HSF1 or Nrf2 decreased SFN-induced HSP70 in the OGD cells. Moreover, knockdown of HSP70 blocked the pro-survival and anti-inflammatory effect of SFN for OGD cells. Moreover, HSP70 overexpression was sufficient to decrease pro-inflammatory cytokines and improve cell survival under OGD. Taken together, PMSNs transported sufficient SFN to the infarcted area in MI. We demonstrated that SFN exerted cardioprotective effect toward MI injury by up-regulating HSP70 through Nrf2/HSF1.

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“…Neutralization of TNF has also been recorded to have positive unintended consequences; patients with rheumatoid arthritis treated with anti‐TNF agents had a lower incidence of cardiovascular events and improved insulin resistance (Barnabe et al., 2011 ; Gonzalez‐Gay et al., 2006 ; Jacobsson et al., 2005 ; Kiortsis et al., 2005 ; van Eijk et al., 2009 ). Work with experimental animal models has shown that TNF neutralization is an effective therapeutic in heart disease and neurodegenerative diseases like Alzheimer's disease (Csiszar et al., 2007 ; Moe et al., 2004 ; Shamim & Laskowski, 2017 ; Toufektsian et al., 2008 ; Wolfe & Michaud, 2004 ). Thus, TNF inhibitors, along with other immune modulators, have possible prophylactic roles that we do not yet fully comprehend.…”

Section: Discussionmentioning

confidence: 99%

Chronic TNF exposure induces glucocorticoid‐like immunosuppression in the alveolar macrophages of aged mice that enhances their susceptibility to pneumonia

Kruckow,

Murray,

Shayhidin

et al. 2024

Aging Cell

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Chronic low‐grade inflammation, particularly elevated tumor necrosis factor (TNF) levels, occurs due to advanced age and is associated with greater susceptibility to infection. One reason for this is age‐dependent macrophage dysfunction (ADMD). Herein, we use the adoptive transfer of alveolar macrophages (AM) from aged mice into the airway of young mice to show that inherent age‐related defects in AM were sufficient to increase the susceptibility to Streptococcus pneumoniae, a Gram‐positive bacterium and the leading cause of community‐acquired pneumonia. MAPK phosphorylation arrays using AM lysates from young and aged wild‐type (WT) and TNF knockout (KO) mice revealed multilevel TNF‐mediated suppression of kinase activity in aged mice. RNAseq analyses of AM validated the suppression of MAPK signaling as a consequence of TNF during aging. Two regulatory phosphatases that suppress MAPK signaling, Dusp1 and Ptprs, were confirmed to be upregulated with age and as a result of TNF exposure both ex vivo and in vitro. Dusp1 is known to be responsible for glucocorticoid‐mediated immune suppression, and dexamethasone treatment increased Dusp1 and Ptprs expression in cells and recapitulated the ADMD phenotype. In young mice, treatment with dexamethasone increased the levels of Dusp1 and Ptprs and their susceptibility to infection. TNF‐neutralizing antibody reduced Dusp1 and Ptprs levels in AM from aged mice and reduced pneumonia severity following bacterial challenge. We conclude that chronic exposure to TNF increases the expression of the glucocorticoid‐associated MAPK signaling suppressors, Dusp1 and Ptprs, which inhibits AM activation and increases susceptibility to bacterial pneumonia in older adults.

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A Single Intravenous sTNFR-Fc Administration at the Time of Reperfusion Limits Infarct Size—Implications in Reperfusion Strategies in Man

Cited by 12 publications

References 28 publications

Serotonin reuptake inhibitor antidepressants (SSRIs) against atherosclerosis

Serotonin reuptake inhibitor antidepressants (SSRIs) against atherosclerosis

Porous magnetic Silica nanoparticles loaded with sulforaphane mitigate myocardial infarction injury through upregulating HSP70

Chronic TNF exposure induces glucocorticoid‐like immunosuppression in the alveolar macrophages of aged mice that enhances their susceptibility to pneumonia

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