Thioredoxin, adiponectin and clinical course of acute fulminant myocarditis

Choi, Jin Oh; Yun, Soo Hyeon; Sung, Kiick; Lee, Young Tak; Park, Joong Il; Ju, Eun Jin; Lee, Sang‐Chol; Park, Seung Woo; Kim, Duk Kyung; Oh, Jae K.; Jeon, Eun Seok

doi:10.1136/hrt.2010.219568

Cited by 11 publications

(7 citation statements)

References 26 publications

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“…Experimental studies indicated that Trx-1 overexpression protects against cardiac cell apoptosis and is associated with good cardiac function in animal models of HF [14,23]. Trx-1 is reportedly rapidly released into the circulation from the damaged cardiomyocytes [24,25], and is increased with advancing CHF severity [9]. Here we showed for the first time that plasma Trx-1 is an independent predictor of future cardiac events.…”

Section: Oxidative Stress and Heart Failuresupporting

confidence: 49%

Association of plasma thioredoxin-1 with renal tubular damage and cardiac prognosis in patients with chronic heart failure

Otaki

Watanabe

Takahashi

et al. 2014

Journal of Cardiology

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Section: Oxidative Stress and Heart Failuresupporting

confidence: 49%

Association of plasma thioredoxin-1 with renal tubular damage and cardiac prognosis in patients with chronic heart failure

Otaki

Watanabe

Takahashi

et al. 2014

Journal of Cardiology

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“…In addition, severity of myocarditis, an inflammation of the heart most likely due to virus infection (395), is correlated to Trx1. In mouse models and patients, Trx1 was up-regulated in the acute stage (505,708) and enhanced in plasma in more severe forms of myocarditis, respectively (129,546). Temocapril treatment of rats in the beginning of experimental autoimmune myocarditis ameliorated the severity via up-regulation of Trx1 in the acute phase (858).…”

Section: Cardiovascular Systemmentioning

confidence: 99%

Thioredoxins, Glutaredoxins, and Peroxiredoxins—Molecular Mechanisms and Health Significance: from Cofactors to Antioxidants to Redox Signaling

Hanschmann

Godoy

Berndt

et al. 2013

Antioxidants & Redox Signaling

581

532

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Thioredoxins (Trxs), glutaredoxins (Grxs), and peroxiredoxins (Prxs) have been characterized as electron donors, guards of the intracellular redox state, and "antioxidants". Today, these redox catalysts are increasingly recognized for their specific role in redox signaling. The number of publications published on the functions of these proteins continues to increase exponentially. The field is experiencing an exciting transformation, from looking at a general redox homeostasis and the pathological oxidative stress model to realizing redox changes as a part of localized, rapid, specific, and reversible redox-regulated signaling events. This review summarizes the almost 50 years of research on these proteins, focusing primarily on data from vertebrates and mammals. The role of Trx fold proteins in redox signaling is discussed by looking at reaction mechanisms, reversible oxidative post-translational modifications of proteins, and characterized interaction partners. On the basis of this analysis, the specific regulatory functions are exemplified for the cellular processes of apoptosis, proliferation, and iron metabolism. The importance of Trxs, Grxs, and Prxs for human health is addressed in the second part of this review, that is, their potential impact and functions in different cell types, tissues, and various pathological conditions.

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“…An investigation into the etiology of FM demonstrates disturbances in the immune system, overstimulation, and disrupted cytokines and chemokines profiles, is critical. 129 Upregulated cytokines or chemokines are the natural reaction against infection but a huge disturbance of immune homeostasis can lead to organ damage. Pro-inflammatory cytokines like IL-1, IL-6, CD-40, and TNF-α, as well as and anti-inflammatory cytokines including sTNFR and IL-10, are elevated in the serum of FM patients.…”

Section: Figmentioning

confidence: 99%

Fulminant myocarditis: a comprehensive review from etiology to treatments and outcomes

Hang

Chen

Seubert

et al. 2020

Sig Transduct Target Ther

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Fulminant myocarditis (FM) is characterized by a rapid progressive decline in cardiac function and a high mortality rate. Since the first report of FM patients in the 1980s, several clinical trials and research studies have been published increasing our knowledge regarding FM. Currently, the diagnosis of FM depends on various techniques including electrocardiography, echocardiography, endomyocardial biopsy, and cardiac magnetic resonance. The development of mechanical circulation support (MCS) devices and progress in our understanding of the pathophysiological mechanisms underlying FM, treatment regimens have evolved from simple symptomatic treatment to a life support-based comprehensive treatment approach. The core mechanism underlying the development of FM is the occurrence of an inflammatory cytokine storm. This review provides a comprehensive account of the current understanding of FM pathophysiology and knowledge regarding its etiology, pathophysiology, treatments, and outcomes.

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Thioredoxin, adiponectin and clinical course of acute fulminant myocarditis

Abstract: In patients with acute myocarditis, the plasma thioredoxin level was increased in the more severe form, and a reduced level of adiponectin was closely correlated with worse short-term outcome in patients with FM.

Cited by 11 publications

References 26 publications

Association of plasma thioredoxin-1 with renal tubular damage and cardiac prognosis in patients with chronic heart failure

Association of plasma thioredoxin-1 with renal tubular damage and cardiac prognosis in patients with chronic heart failure

Thioredoxins, Glutaredoxins, and Peroxiredoxins—Molecular Mechanisms and Health Significance: from Cofactors to Antioxidants to Redox Signaling

Fulminant myocarditis: a comprehensive review from etiology to treatments and outcomes

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