The association of plasma kynurenines with risk of acute myocardial infarction in patients with stable angina pectoris

Pedersen, Eva Ringdal; Tuseth, Nora; Eussen, Simone J. P. M.; Ueland, Per Magne; Svingen, G.F.T.; Schartum-Hansen, Hall; Seifert, Reinhard; Midttun, Øivind; Meyer, Klaus; Nygård, Ottar

doi:10.1016/j.atherosclerosis.2014.05.406

Cited by 2 publications

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“…33 In the present study, kynurenine was associated with CRP, as were some metabolites of the kynurenine pathway in previous studies. 30 Given that inflammation is associated with muscle dysfunction 34, 35 and reduced functional capacity, 36 inflammation may be a common background both for higher kynurenine and impaired functional capacity observed in the present study. Kynurenine is an endothelium-derived relaxing factor 37 and may also be produced as a feedback mechanism to counteract vasoconstriction, 21,38 which is frequently observed and measured as elevated systemic vascular resistance in right heart catheterization in patients with HF.…”

Section: Potential Mechanismsmentioning

confidence: 91%

“…For example, Pedersen et al advocated that the kynurenine-tryptophan ratio may be ideal to estimate the inflammatory activity. 30 Because HFpEF and HFrEF have distinct phenotypes, the association between kynurenine level and muscle strength/ functional capacity may be different between these 2 subgroups. Indeed, skeletal muscle strength was inversely associated with kynurenine level in HFrEF patients but not in HFpEF patients.…”

Section: Study Limitationsmentioning

confidence: 99%

“…In contrast, in most previous studies, inflammatory processes were regarded as the principal pathophysiological mechanism in patients with activated kynurenine pathway. 21,29, 30 In the previous studies kynurenine-tryptophan ratio was treated as an established marker of interferon (IFN)-γ activity and T-helper 1 immune responses 21,26 because the degradation from tryptophan into kynurenine is mediated mainly by indolamine 2,3-dioxygenase, which is not expressed unless stimulated by IFN-γ (Figure 4). Katz et al, however, advocated that the role of kynurenine metabolites in immune response and inflammation may not be simple, 31,32 referring to the notion that depletion of tryptophan from T cells and/or tryptophan metabolites themselves might make T cells unable to trigger the appropriate immune reaction.…”

Section: Potential Mechanismsmentioning

confidence: 99%

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Impact of Plasma Kynurenine Level on Functional Capacity and Outcome in Heart Failure　― Results From Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF) ―

Konishi

Ebner

Springer

et al. 2017

Circ J

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Background: Kynurenine is a circulating metabolite from the essential amino acid tryptophan. Accelerated degradation of kynurenine in skeletal muscle has been reported to provide an anti-inflammatory effect. The aim of this study was to investigate the association between blood kynurenine and muscle mass/function in patients with heart failure (HF), in whom diseased muscle mass/ function plays a pathophysiological role. Methods and Results:Plasma kynurenine was assessed in 249 patients with HF (67±11 years, 21% women) and in 45 controls from the SICA-HF study. Kynurenine was higher in 173 HF patients with reduced ejection fraction (EF) and in 76 patients with preserved EF than controls (3.5±1.5, 3.4±1.3, and 2.4±1.1 μmol/L, P<0.001). In HF patients, kynurenine had an inverse association with handgrip strength (r=-0.26, P<0.01), peak oxygen consumption (r=-0.29, P<0.01), 6-min walk distance (r=-0.23, P<0.01), and had a positive association with kidney and liver function parameters. No correlation was observed between kynurenine and lean mass. On multivariable linear regression analysis, a significant association was noted between kynurenine and peak oxygen consumption even after adjustment for age, gender, BMI, and hemoglobin (β=-0.23, P<0.001). Patients with higher kynurenine were at higher risk of death (adjusted HR, 1.46 per 1 μmol/L, P<0.01). Conclusions:In stable HF patients, plasma kynurenine was inversely correlated with muscle strength and functional capacity as well as with liver and kidney function.

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Section: Potential Mechanismsmentioning

confidence: 91%

Section: Study Limitationsmentioning

confidence: 99%

Section: Potential Mechanismsmentioning

confidence: 99%

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Impact of Plasma Kynurenine Level on Functional Capacity and Outcome in Heart Failure　― Results From Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF) ―

Konishi

Ebner

Springer

et al. 2017

Circ J

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“…Отношение Кин/Три обнаружило предиктовые значения при кардиоваскулярной смертности у пациентов со стабильным заболеванием коро-нарной артерии [53]. Уровень катаболитов Кин был повышен у пациентов со стабильной сте-нокардией и был предиктором риска развития острого инфаркта миокарда [54].…”

Section: клеточные механизмы защиты от триптофано-вого «голода»unclassified

Tryptophan and Indoleamine-2,3-Dioxygenase (Ido) in Pathogenesis of Immunosuppressive Clinical Conditions

Козлов¹,

Демина²

2017

Med. immunol.

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Адрес для переписки:Козлов Владимир Александрович ФГБНУ «Научно-исследовательский институт фундаментальной и клинической иммунологии» 630099, Россия, г. Новосибирск, ул. Ядринцевская, 14. Тел.: 8 (383) 222-66-27. Факс: 8 (383) 222-70-28. E-mail: vakoz40@yandex.ru Address for correspondence : Kozlov Vladimir A. Research Institute of Fundamental and Clinical Immunology 630099, Russian Federation, Novosibirsk, Yadrintsevskaya str., Образец цитирования: иммунология, 2017. Т. 19, № 3. С. 225-240. doi: 10.15789/1563-0625-2017-3-225-240 © Козлов В.А., Демина Д.В., 2017 For citation: V. A. Kozlov, Immunologiya, 2017, Vol. 19, no. 3, pp. 225-240. doi: 10.15789/1563-0625-2017-3-225-240 DOI: 10.15789/1563-0625-2017 ТРИПТОФАН И INDOLEAMINE-2,3-DIOXYGENASE (IDO) В ПАТОГЕНЕЗЕ ИММУНОКОМПРОМЕТИРОВАННЫХ ЗАБОЛЕВАНИЙКозлов В.А., Демина Д.В. ФГБНУ «Научно-исследовательский институт фундаментальной и клинической иммунологии», г. Новосибирск, РоссияРезюме. Все больше и больше литературных данных свидетельствуют о ведущей роли в форми-ровании иммуносупрессорных механизмов фермента indoleamin 2,3-deoxygenase (IDO), которая продуцируется в основном дендритными клетками, в индукции которой участвует в основном IFNγ и функции которой состоят в индукции катаболизма незаменимой аминокислоты триптофана. Уже одно снижение уровня триптофана в околоклеточной среде обуславливает подавление ряда функ-ций клеток иммунной системы и индукцию регуляторных Т-клеток. Появление ряда катаболитов триптофана еще более усугубляет иммунодепрессивное состояние, индуцированное повышенной экспрессией IDO. Предполагается, что цепочка из IDO, триптофана и его катаболитов в значитель-ной степени определяет формирование гиперсупрессорного состояния при опухолевом росте и гипо-(или недостаточного) супрессорного состояния при аутоиммунных и аллергических заболеваниях. Отсюда вытекают и новые задачи в терапии: найти способы терапии, направленные на снижение ак-тивности фермента IDO, участвующего в индукции клеток-супрессоров при опухолевом росте, и в то же время направленные на стимуляцию активности данного фермента для повышения супрессорной активности регуляторных клеток. that the interactions between IDO, tryptophan and its catabolites largely determine a development of hypersuppressor state in tumor growth and a hypo-(or lack of) suppressor status in autoimmune and allergic diseases. This implies some novel tasks for the therapy, including a treatment aimed for reduction of the IDO activity since the latter is involved in suppressor cell induction during tumor growth. Respectively, stimulation of IDO activity may augment suppressor activity of the regulatory cells. Ключевые слова: иммунопатология, иммуносупрессия, триптофан, indoleamine 2,3-dioxygenase, кинуренин TRYPTOPHAN AND INDOLEAMINE-2,3-DIOXYGENASE (IDO) IN PATHOGENESIS OF IMMUNOSUPPRESSIVE CLINICAL CONDITIONS

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The association of plasma kynurenines with risk of acute myocardial infarction in patients with stable angina pectoris

Cited by 2 publications

References 0 publications

Impact of Plasma Kynurenine Level on Functional Capacity and Outcome in Heart Failure　― Results From Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF) ―

Impact of Plasma Kynurenine Level on Functional Capacity and Outcome in Heart Failure　― Results From Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF) ―

Tryptophan and Indoleamine-2,3-Dioxygenase (Ido) in Pathogenesis of Immunosuppressive Clinical Conditions

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The association of plasma kynurenines with risk of acute myocardial infarction in patients with stable angina pectoris

Cited by 2 publications

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Impact of Plasma Kynurenine Level on Functional Capacity and Outcome in Heart Failure ― Results From Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF) ―

Impact of Plasma Kynurenine Level on Functional Capacity and Outcome in Heart Failure ― Results From Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF) ―

Tryptophan and Indoleamine-2,3-Dioxygenase (Ido) in Pathogenesis of Immunosuppressive Clinical Conditions

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Impact of Plasma Kynurenine Level on Functional Capacity and Outcome in Heart Failure　― Results From Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF) ―

Impact of Plasma Kynurenine Level on Functional Capacity and Outcome in Heart Failure　― Results From Studies Investigating Co-morbidities Aggravating Heart Failure (SICA-HF) ―