TNF-  down-regulates sarcoplasmic reticulum Ca2+ ATPase expression and leads to left ventricular diastolic dysfunction through binding of NF- B to promoter response element

Tsai, Chia Ti; Wu, Cho Kai; Lee, Jen Kuang; Chang, Sheng‐Nan; Kuo, Yu Min; Wang, Yi Chih; Lai, Ling‐Ping; Chiang, Fu-Tien; Hwang, Juey Jen; Lin, Jiunn Lee

doi:10.1093/cvr/cvv008

Cited by 46 publications

(41 citation statements)

References 39 publications

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“…1,2,5 Various animal models have been used in the study of LVDD, including the mRen2.Lewis rats, 9,10 deoxycorticosterone acetate-hypertensive rats, 30 spontaneously hypertensive rats (SHR), 31 streptozotocin and a high-fat diet-induced diabetic rats and mice, 32,33 lipopolysaccharide-induced high inflammation and LVDD, 34 and aortocaval fistula-induced volume overload model. 35 However, all these animal models are pathological models and may not reflect the biological conditions of LVDD that exist in healthy, aging women after the cessation of ovarian estrogen production.…”

Section: Discussionmentioning

confidence: 99%

Mast Cell Inhibition Attenuates Cardiac Remodeling and Diastolic Dysfunction in Middle-aged, Ovariectomized Fischer 344 × Brown Norway Rats

Wang

Alencar

et al. 2016

Journal of Cardiovascular Pharmacology

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The incidence of left ventricular diastolic dysfunction (LVDD) increases in women following menopause, yet the mechanisms are unclear. Because mast cells participate in the pathological processes of various cardiac diseases, we hypothesized that mast cell inhibition would protect against estrogen loss-induced LVDD. The mast cell stabilizer, cromolyn sodium (30 mg/kg/day), or vehicle was administered subcutaneously by osmotic minipump to ovariectomized (OVX) female Fischer344×Brown Norway (F344BN) rats starting at four weeks after surgery. Eight weeks after OVX, systolic blood pressure increased by 20% in OVX vs. sham rats, and this effect was attenuated after four weeks of cromolyn treatment. Also, cromolyn mitigated the adverse reductions in myocardial relaxation (e′) and increases in left ventricle (LV) filling pressures (E/e′), LV mass, wall thicknesses, and interstitial fibrosis from OVX. While cardiac mast cell number was increased after OVX, cardiac chymase activity was not overtly altered by estrogen status and tended to decrease by cromolyn. Contrariwise, Ang II content was greater in hearts of OVX vs. sham rats, and cromolyn attenuated this effect. Taken together, mast cell inhibition with cromolyn attenuates LV remodeling and LVDD in OVX-F344BN rats possibly through actions on the heart level and/or via vasodilatory effects at the vascular level.

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Section: Discussionmentioning

confidence: 99%

Mast Cell Inhibition Attenuates Cardiac Remodeling and Diastolic Dysfunction in Middle-aged, Ovariectomized Fischer 344 × Brown Norway Rats

Wang

Alencar

et al. 2016

Journal of Cardiovascular Pharmacology

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“…ФНО-α является одним из основных медиаторов иммун-ного ответа. Кардиомиоциты способны индуцировать ФНО-α при напряжении стенки миокарда (диастоличе-ском стрессе), при этом чем выше уровень конечного диастолического давления в ЛЖ, тем больше количество производимого цитокина [38]. Большая степень умень-шения полостей сердца во II группе может объяснить воз-можный механизм более выраженного снижения ФНО-α.…”

Section: Discussionunclassified

Biochemical aspects of gender differences in response to cardiac resynchronization therapy

Enina¹,

Кузнецов²,

Солдатова³

et al. 2017

RHJ

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“…Supporting data has been provided by another transgenic line of mice from Feldman's laboratory, demonstrating that overproduction of TNF-α by cardiac myocytes was enough to cause dilated cardiomyopathy [42]. In rat and dog hearts, in vivo administration of exogenous TNF-α, dose dependently reduced sarcoplasmic reticulum Ca 2+ uptake and myofilament Ca 2+ sensitivity leading to cardiodepressant effects [43]. As a result of extrapolation of findings from experimental animals, it was assumed that TNF-α is deleterious and by virtue of its deleterious effects to myocardial function in humans it can contribute to pathogenesis of heart disease.…”

Section: Tnf-α and Cardiac Injurymentioning

confidence: 97%

Tumor Necrosis Factor-Alpha and Inflammation-Mediated Cardiac Injury

Howerton¹,

Tarzami²

2017

J Cell Sci Ther

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Experimental evidence is accumulating implicating a major role for inflammatory activation in chronic heart failure. Levels of pro-inflammatory protein mediators, such as tumor necrosis factor-alpha (TNF-α), a pro inflammatory cytokine, have been shown to be elevated in heart failure patients and appear to be directly related to pathological changes in the myocardium. Unfortunately, outcomes from clinical trials using anti-cytokine therapies to chronic heart failure patients have been largely disappointing. TNF-α is a pleiotropic cytokine, impacting tissues in a complex manner that regulates many physiological and pathological processes that can trigger differentiation, inflammation, and cell death. TNF-α is important in initiating and regulating the cytokine cascade during an inflammatory response. Most of the studies focused on the TNF-α as an immune mediator but its function in cardiac cells is not well defined. This review focuses on the role of TNF-α in acute and/or chronic cardiac conditions. We will discuss the problem with the current anti-cytokine therapies and potential problems underlying their lack of success so far.

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TNF- down-regulates sarcoplasmic reticulum Ca2+ ATPase expression and leads to left ventricular diastolic dysfunction through binding of NF- B to promoter response element

Abstract: TNF-α suppresses SERCA2a gene expression via the IKK/IκB/NF-κB pathway and binding of NF-κB to the SERCA2a gene promoter, and its effect is blocked by simvastatin, demonstrating the potential therapeutic effect of statins in treating inflammation-related diastolic dysfunction.

Cited by 46 publications

References 39 publications

Mast Cell Inhibition Attenuates Cardiac Remodeling and Diastolic Dysfunction in Middle-aged, Ovariectomized Fischer 344 × Brown Norway Rats

Mast Cell Inhibition Attenuates Cardiac Remodeling and Diastolic Dysfunction in Middle-aged, Ovariectomized Fischer 344 × Brown Norway Rats

Biochemical aspects of gender differences in response to cardiac resynchronization therapy

Tumor Necrosis Factor-Alpha and Inflammation-Mediated Cardiac Injury

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