TNF-induced cardiomyopathy

Hegewisch, S.

doi:10.1016/0140-6736(90)90115-l

Cited by 166 publications

(57 citation statements)

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“…Myocardial expression of TNF-␣ mRNA copies corrected for ␤-actin mRNA copies was increased in MR patients (38.96Ϯ42.74ϫ10 6 ) compared with otherwise healthy donor hearts (0.88Ϯ0.75ϫ10 6 , Pϭ0.01). There was a trend toward a correlation between the plasma TNF-␣ levels and myocardial TNF-␣ gene expression (rϭ0.47, Pϭ0.15, Figure 2A), but not with its receptors.…”

Section: Myocardial Tnf-␣ Gene Expression In Mr Patients and Normal Dmentioning

confidence: 98%

Myocardial Proinflammatory Cytokine Expression and Left Ventricular Remodeling in Patients With Chronic Mitral Regurgitation

et al. 2003

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Background-In an animal model, stretch was shown to induce myocardial tumor necrosis factor-␣ (TNF-␣) expression.The purposes of this study were to determine whether the left ventricular (LV) volume overload that occurs in patients with chronic mitral regurgitation (MR) can induce myocardial and systemic TNF-␣ expression and whether there is a relationship between TNF-␣ expression and LV remodeling. Methods and Results-Plasma TNF-␣ and its receptors were measured before mitral valve (MV) repair surgery in 26 MR patients and 23Ϯ12 months after MV repair surgery in 9 MR patients. Myocardial mRNA copies of TNF-␣ were determined in 11 MR and 10 donor hearts using quantitative RT-PCR. Compared with 15 control subjects, pre-MV repair plasma TNF-␣ (3.59Ϯ1.81 versus 2.03Ϯ1.02 pg/mL, PϽ0.005) and its receptor levels were elevated in MR patients. Myocardial TNF-␣ mRNA copies (corrected for ␤-actin mRNA expression) in MR patients and donor hearts were 38.96Ϯ42.74ϫ10 6 and 0.88Ϯ0.75ϫ10 6 , respectively (Pϭ0.01). After MV surgery, there was a decrease in the plasma levels of TNF-␣ (2.79Ϯ1.14 versus 3.51Ϯ1.34 pg/mL, Pϭ0.02) and its receptors. There was a correlation between myocardial TNF-␣ expression and preoperative LV end-diastolic and end-systolic volumes. Moreover, there was an inverse correlation between myocardial TNF-␣ expression and regression in LV end-diastolic (rϭϪ0.76, Pϭ0.007) and end-systolic (rϭϪ0.73, Pϭ0.01) volumes after MV surgery. Conclusions-TNF-␣

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Section: Myocardial Tnf-␣ Gene Expression In Mr Patients and Normal Dmentioning

confidence: 98%

Myocardial Proinflammatory Cytokine Expression and Left Ventricular Remodeling in Patients With Chronic Mitral Regurgitation

et al. 2003

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“…For example, TNF-␣ levels are markedly elevated in advanced heart failure, 5,6 and in experimental settings, TNF-␣ can produce left ventricular dysfunction, 7 pulmonary edema, 8,9 and cardiomyopathy. 10 Furthermore, TNF-␣ is upregulated in the myocardium in response to both transient myocardial ischemia and reperfusion, [11][12][13][14] and it has been hypothesized that persistent overexpression of TNF-␣ after ischemia might lead to adverse coronary outcomes. 15 However, although some studies suggest that TNF-␣ levels increase acutely with coronary ischemia, 16,17 it is unknown whether elevations of TNF-␣ measured several months after myocardial infarction (MI) are associated with increased risk of recurrent coronary events.…”

mentioning

confidence: 99%

Elevation of Tumor Necrosis Factor-α and Increased Risk of Recurrent Coronary Events After Myocardial Infarction

Ridker¹,

Rifai²,

Pfeffer³

et al. 2000

Circulation

854

475

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MD; for the Cholesterol And Recurrent Events (CARE) InvestigatorsBackground-Levels of tumor necrosis factor-␣ (TNF-␣) increase with acute ischemia. However, whether elevations of TNF-␣ in the stable phase after myocardial ischemia (MI) are associated with increased risk of recurrent coronary events is unknown. Methods and Results-A nested case-control design was used to compare TNF-␣ levels obtained an average of 8.9 months after initial MI among 272 participants in the Cholesterol And Recurrent Events (CARE) trial who subsequently developed recurrent nonfatal MI or a fatal cardiovascular event (cases) and from an equal number of age-and sex-matched participants who remained free of these events during follow-up (controls). Overall, TNF-␣ levels were significantly higher among cases than controls (2.84 versus 2.57 pg/mL, Pϭ0.02). The excess risk of recurrent coronary events after MI was predominantly seen among those with the highest levels of TNF-␣, such that those with levels in excess of 4.17 pg/mL (the 95th percentile of the control distribution) had an Ϸ3-fold increase in risk (RRϭ2.7, 95% CI 1.4 to 5.2, Pϭ0.004). Risk estimates were independent of other risk factors and were similar in subgroup analyses limited to cardiovascular death (RRϭ2.1) or to recurrent nonfatal MI (RRϭ3.2). Conclusions-Plasma concentrations of TNF-␣ are persistently elevated among post-MI patients at increased risk for recurrent coronary events. These data support the hypothesis that a persistent inflammatory instability is present among stable patients at increased vascular risk. Novel therapies designed to attenuate inflammation may thus represent a new direction in the treatment

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“…16) Systemic administration of recombinant TNF-α has consistently resulted in myocardial depression of myocyte contractility 17) and has been associated with the development of cardiomyopathy. 18) In the present study, we introduce CP as antiinflammation strategy in rats with myocardial ischemia reperfusion. We confirmed the effects of CP on TNF-α production in cardiac myocytes by immunohistochemistry staining and that TNF-α staining was less intensive with CP treatment.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of TNF-^|^alpha; by Cyclophosphamide Reduces Myocardial Injury After Ischemia-Reperfusion

Jin

Chen

Wang

et al. 2013

ATCS

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Purpose: The purpose of this study was to determine whether cyclophosphamide (CP) can decrease myocardial and systemic TNF-αexpression and thus protects myocardial I/R injury. Methods: Open chest rats were subjected to 30 min of ischemia followed by 3h, 12h or 24h of reperfusion. Rats were divided into sham group, I/R group and CP group, and each group included 3 timepoint subgroups (3h, 12h and 24h). Plasma TNF-αwas measured by cytometric bead array (CBA) and immunohistochemistry was used to detect TNF-α in myocardium. Results: Compared with I/R group, rats treated with CP showed a significant difference with decreased plasma TNF-α (13.31 ± 2.62 vs 14.13 ± 5.95 pg/mL at 3 h reperfusion, 10.1 ± 2.73 vs 12.54 ± 5.00 pg/mL at 12 h reperfusion, 10.38 ± 5.59 vs 13.00 ± 3.59 pg/mL at 24 h reperfusion, p <0.05 respectively). Immunostaining was less intense with CP injection at each reperfusion time. The score of the intensity of myocardial TNF-αstaining was down regulated. Conclusions: TNF-α is expressed in the myocardium and plasma after myocardial I/R injury. CP might be a feasible strategy for anti-TNF-α to protect myocardial I/R injury.Keywords: cyclophosphamide, TNF-α, ischemia/reperfusion appeared to be associated with a reduced risk of cardiovascular disease. 1) We recently also disclosed that cyclophosphamide (CP) could improve myocardial function in rats after ischemia reperfusion injury. These findings could help to gain some insight into therapeutic potential of CP in myocardial I/R injury.2) However, the mechanism remains unclear. As we have known TNF-αis released during myocardial I/R from storage sites in tissue mast cells within the myocardium 3) and possibly also from cardiomyocyte itself 4) and the plasma inflammatory cells.5) Presently, we used open-chest ischemia-reperfusion rat model with minimal surgical trauma to further demonstrate whether down-regulation with TNF-α-related inflammatory pathways by CP could reduce myocardial injury after I/R.

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TNF-induced cardiomyopathy

Cited by 166 publications

References 0 publications

Myocardial Proinflammatory Cytokine Expression and Left Ventricular Remodeling in Patients With Chronic Mitral Regurgitation

Myocardial Proinflammatory Cytokine Expression and Left Ventricular Remodeling in Patients With Chronic Mitral Regurgitation

Elevation of Tumor Necrosis Factor-α and Increased Risk of Recurrent Coronary Events After Myocardial Infarction

Inhibition of TNF-^|^alpha; by Cyclophosphamide Reduces Myocardial Injury After Ischemia-Reperfusion

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