Translational overview of cytokine inhibition in acute myocardial infarction and chronic heart failure

Hartman, Minke H. T.; Groot, Hilde E.; Leach, Irene Mateo; Karper, J.C.; Harst, Pim van der

doi:10.1016/j.tcm.2018.02.003

Cited by 74 publications

(57 citation statements)

References 100 publications

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“…There have been several strategies proposed to inhibit post-MI inflammation, but early attempts have often resulted in adverse outcomes in clinical trials [38,85]. On the other hand, approaches that focus on resolving post-MI inflammation have been sparsely used [50].…”

Section: Resolution Of Inflammationmentioning

confidence: 99%

Immune responses in cardiac repair and regeneration: a comparative point of view

Lai

Marín-Juez

Stainier

2018

Cell. Mol. Life Sci.

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Immediately after cardiac injury, the immune system plays major roles in repair and regeneration as it becomes involved in a number of processes including damage-associated signaling, inflammation, revascularization, cardiomyocyte dedifferentiation and replenishment, and fibrotic scar formation/resolution. Recent studies have revealed that different immune responses occur in the various experimental models capable or incapable of cardiac regeneration, and that harnessing these immune responses might improve cardiac repair. In light of this concept, this review analyzes current knowledge about the immune responses to cardiac injury from a comparative perspective. Insights gained from such comparative analyses may provide ways to modulate the immune response as a potential therapeutic strategy for cardiac disease.

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Section: Resolution Of Inflammationmentioning

confidence: 99%

Immune responses in cardiac repair and regeneration: a comparative point of view

Lai

Marín-Juez

Stainier

2018

Cell. Mol. Life Sci.

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“…Роль ФНО-α в развитии ХСН общепризнана [38]. В общей популяции высокий уровень ФНО-α является предиктором развития ХСН, у пациентов с ХСН его концентрация коррелирует с ФК по NYHA.…”

Section: ингибиторы фно-αunclassified

“…Выраженная связь между уровнем провоспалительных цитокинов и риском развития ХСН или ее клиническим ухудшением позволила предположить, что фармакологическая блокада цитокинов может оказаться эффективным средством профилактики и лечения ХСН, особенно, у пациентов с хроническими системными воспалительными заболеваниями [37,38]. При развитии ФНО-α-индуцированной модели ремоделирования миокарда в начале заболевания существует терапевтическое окно, в течение которого процессы, ведущие к интерстициальному фиброзу, могут быть прекращены или замедлены [39].…”

Section: ингибиторы фно-αunclassified

“…Описаны и другие плеотропные эффекты иФНО-α -улучшение эндотелиальной, микроваскулярной функции, функции левого предсердия и ФВЛЖ [40]. В нескольких РКИ на небольшом количестве пациентов с ХСН отмечено улучшение ФВЛЖ, сосудорасширяющих свойств эндотелия на фоне этанерцепта CHF in Rheumatoid Arthritis Patients ХСН у больных ревматоидным артритом [38]. Это послужило теоретической основой для двух сходных по дизайну, двойных слепых, плацебо-контролируемых РКИ (RENAISSANCE и RECOVER), в которых оценивали пользу ингибирования ФНО-α этанерцептом у больных тяжелой ХСН.…”

Section: ингибиторы фно-αunclassified

“…Интерлейкин 1β -провоспалительный цитокин, высвобождаемый активированными моноцитами/ макрофагами после расщепления своего аминоконцевого участка каспазой-1. Этот цитокин участвует в патогенезе целого ряда ревматических заболеваний, стимулируя выработку матриксных металлопротеиназ, молекул адгезии, других цитокинов в синовиальной и хрящевой ткани [22,36,38]. Изначально анакинра (рекомбинантный антагонист рецептора к ИЛ-1) была одобрена для лечения больных РА, однако сравнение препарата с иФНО-α продемонстрировало большую эффективность последних.…”

Section: ингибирование ил-1βunclassified

See 2 more Smart Citations

Chronic Heart Failure in Rheumatoid Arthritis Patients (Part III): Effects of Antirheumatic Drugs

Новикова¹,

Udachkina²,

Kirillova³

et al. 2020

Racionalʹnaâ farmakoterapiâ v kardiologii

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Chronic autoimmune inflammation is one of the leading risk factors for the development of chronic heart failure (CHF) in rheumatoid arthritis (RA). The purpose of the review is to analyze the results of investigations on the effects of conventional synthetic disease-modifying anti-rheumatic drugs (csDMARDs), biological disease-modifying anti-rheumatic drugs (bDMARDs), and targeted csDMARDs on cardiac function and the risk of developing CHF in patients with RA. Methotrexate may reduce the CHF risk and have a positive effect on the course of this condition in patients with RA. Despite the data on the presence of leflunomide effects that impede myocardial remodeling, there is no evidence of the role of the drug in the prevention of CHF in RA patients. Hydroxychloroquine may contribute to the prevention of CHF, but the risk of developing severe cardiotoxicity should be considered when taking the drug for a long time. Most studies have not revealed the negative effect of tumor necrosis factor inhibitors on the prevalence and incidence of new cases of CHF in RA patients, and an improvement in the structure and function of the heart during therapy has been shown. Inhibitors of interleukin (IL) -1, inhibitors of IL-6, inhibitors of T-cell co-stimulation, anti-B-cell therapy, targeted csDMARDs do not increase the risk of CHF and may have cardioprotective effects, including slowing the progression of left ventricle myocardial dysfunction. Due to the high risk of CHF and CHF-associated mortality in RA patients, early diagnosis of cardiac dysfunction, development of a prevention and treatment strategies are needed, including high-quality prospective studies to assess the effect of anti-rheumatic therapy on myocardial function, risk of developing and decompensation of CHF in RA patients. It is possible that some drugs may possess protective effects on cardiomyocytes so they could become the first-line drugs in patients with CHF or the risk of its development.

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Myocardial Dysfunction and Heart Failure in Rheumatoid Arthritis

Park

Griffin

Bathon

2021

Arthritis & Rheumatology

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Rheumatoid arthritis (RA) patients have almost twice the risk of heart failure (HF) as individuals without RA, even with adjustment for the presence of ischemic heart disease. Moreover, RA patients remain at a 2-fold higher risk of mortality from HF compared to non-RA patients. These observations suggest that RA-specific inflammatory pathways are significant contributors to this increased risk of HF. Herein we summarize the epidemiology of HF in RA patients, the differences in myocardial structure or function between RA patients and non-RA patients without clinical signs of HF, and data on the role of systemic and local inflammation in RA HF pathophysiology. We also discuss the impact of subduing inflammation through the use of RA disease-modifying therapies on HF and myocardial structure and function, emphasizing gaps in the literature and areas needing further research.

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Translational overview of cytokine inhibition in acute myocardial infarction and chronic heart failure

Cited by 74 publications

References 100 publications

Immune responses in cardiac repair and regeneration: a comparative point of view

Immune responses in cardiac repair and regeneration: a comparative point of view

Chronic Heart Failure in Rheumatoid Arthritis Patients (Part III): Effects of Antirheumatic Drugs

Myocardial Dysfunction and Heart Failure in Rheumatoid Arthritis

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