Possibility of Inhibition of TNF-α/NF-kB Signaling Pathway Activation in Myocardium and Reverse Cardiac Hemodynamics in Chronic Ischemic Heart Disease

Pa, Galenko-Iaroshevsky; Gv, Sukoyan; Di, Ionov; Av, Zelenskaya; Ng, Khvitia

doi:10.4172/2161-0681.1000310

Cited by 2 publications

(2 citation statements)

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“…В отличие от NTproBNP, редокс-потенциал НАД / НАДН коррелирует с маркером выраженности аутоиммунного процесса, ассоциированного с СД 2 и ХСН, что подтверждается сильной обратной корреляционной взаимосвязью между уровнем редокс-потенциала и гиперобразованием ФНО-α (r = -0,81; р <0,0002). Редокс-потенциал является прямым регулятором посттранскрипционного процесса синтеза данного провоспалительного цитокина [26][27]. Снижение уровня НАД / НАДН, определяемое в плазме крови, не является селективным маркером для повреждения миокарда, а скорее может рассматриваться как интегральный показатель нарушения редокс-баланса органов-мишеней развития СД 2 и ХСН: поджелудочной железы, миокарда, почек, мозга.…”

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Biochemical algorithms of early diagnostic of metabolic remodeling and cardiac hypertrophy in patients with diabetic mellitus and chronic heart failure cause by ischemic heart disease

Донецкая¹,

Шульдешова²,

Tulupova³

et al. 2019

Klinicist

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The aims of study– a development of biochemical algorithms of early diagnostic of severity of CHF in patients with DM and IHD and analyze interrelationships between plasma redox-potential, as a marker of progressive of tissues metabolic remodeling and cardiac hypertrophy and markers of progressive of DM, neurohumoral markers of severity of CHF, and frequency of heart rhythm disturbances.Materials and methods.172 patients, male / female (45–65 years), with diagnosis of DM (metabolic decompensation of carbohydrate metabolism, HbА1c – 7.4 ± 1.9 %) during 3–15 years, accompanied with IHD and symptoms of CHF I–IV NYHA functional class (FC). The first point of investigation was examined markers of DM progression HbА1c, changes in FC of HCHF and evidenced prognostic neurohumoral markers of myocardial dysfunction NT-proBNP, and as a second (surrogate) point – changes in redox-potential NAD / NADH and total pool of pyridine nucleotides.Results.Mean NYHA FC CHF in cohort of DM patients and IHD was 2.4 ± 1.2, mean point of CHF estimated by scale of symptoms of CHF was 6.7 ± 0.6, mean distance in 6-minute test was 212 ± 26 m, concentration of neurohumoral markers of myocardial dysfunction NT-proBNP 178 ± 26 fmol / l at the level of HbA1c = 7.8 ± 1.0 %, mean redox-potential of plasma, НАД / НАДН, 0.71 ± 0.06 and total pool of pyridine nucleotide 15.1 ± 1.2 μmol / mg protein of plasma. For the first time was shown that changes in redox-potential and sum of pyridine nucleotide coupled with severity of CHF (FC of CHF), eliminated the correlation between NAD / NADH and HbA1c (r = –0.79, p<0.001), and NTproBNP (r = –0.73; р <0.001), and increasing of tumor necrosis factor alpha (TNF-α, r = –0.73; р <0.001). Simultaneously maintenance decreasing of NAD / NADH and sum of pyridine nucleotide in plasma of patients with DM and IHD coupled with increasing of daily mean values of paired supraventricular and ventricular extrasystoles.Conclusions.In patients with DM and CHF with left ventricular dysfunction the decreasing of redox-potential level in plasma could be recommended as a markers of increasing of metabolic remodeling and progression of cardiac hypertrophy.

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Section: Discussionunclassified

Biochemical algorithms of early diagnostic of metabolic remodeling and cardiac hypertrophy in patients with diabetic mellitus and chronic heart failure cause by ischemic heart disease

Донецкая¹,

Шульдешова²,

Tulupova³

et al. 2019

Klinicist

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“…The biomechanical reorganization of the heart causes changes in the expression of genes that mediate CSI, apoptotic reactions, etc. [6]. Therefore, it is expedient to study in detail the molecular mechanisms of atherogenesis in order to find new targets for pharmacological effects in CA and CHD.…”

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Systemic Inflammation and the State of Central Hemodynamics in Patients With Coronary Heart Disease

Шуть¹,

Чекаліна

Trybrat

et al. 2018

BMFCM

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Possibility of Inhibition of TNF-α/NF-kB Signaling Pathway Activation in Myocardium and Reverse Cardiac Hemodynamics in Chronic Ischemic Heart Disease

Cited by 2 publications

References 21 publications

Biochemical algorithms of early diagnostic of metabolic remodeling and cardiac hypertrophy in patients with diabetic mellitus and chronic heart failure cause by ischemic heart disease

Biochemical algorithms of early diagnostic of metabolic remodeling and cardiac hypertrophy in patients with diabetic mellitus and chronic heart failure cause by ischemic heart disease

Systemic Inflammation and the State of Central Hemodynamics in Patients With Coronary Heart Disease

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