New insights into the pathogenesis of dilated cardiomyopathy: possible underlying autoimmune mechanisms and therapy

Mobini, Reza; Maschke, Hans E.; Waagstein, Finn

doi:10.1016/j.autrev.2003.10.005

Cited by 43 publications

(28 citation statements)

References 37 publications

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“…The disease progression of DCM is highly diverse due to its aetiological and pathophysiological heterogeneity [1], and now appropriate treatment of DCM remains a major clinical challenge [2]. Although the immunopathogenesis of DCM remains unclear, current clinical and experimental evidence has suggested that immune activation and the consequential inflammatory response in the myocardium may be involved in the development and progression of DCM [3,4].…”

Section: Introductionmentioning

confidence: 99%

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

Li¹,

Zhou²,

Tang³

et al. 2017

Cell Physiol Biochem

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Background/Aims: The imbalance of Treg/Th17 cells plays important role in the pathogenesis of dilated cardiomyopathy (DCM). Response gene to complement (RGC)-32 is a cell cycle regulator that plays an important role in cell proliferation. We evaluated whether the upregulation of RGC-32 was implicated in the homeostasis of Treg/Th17 cells in DCM. Methods:The levels of plasma RGC-32, IL-17 and TGF-β1, and the frequencies of circulating CD4 + RGC-32 + T cells, Th17 and Treg cells in patients with DCM were determined by Cytokinespecific sandwich ELISA and the flow cytometer (FCM), respectively. Results: A significant elevation of plasma RGC-32 in patients with DCM compared with healthy control (HC) subjects was observed. This upregulation was associated with an increase in frequency of Th17 and a decrease in frequency of Treg cells. To further assessed the role of RGC-32, we investigated the effects of RGC-32 up-or down-regulation on frequencies of Th17 and Treg cells in peripheral blood mononuclear cells (PBMCs) from subjects. Importantly, overexpression of RGC-32 was accompanied by an augmentation of Th17 and a reduction of Treg expression. Conclusion: In summary, our study demonstrated the up-regulation of RGC-32 contributed to the imbalance of Treg/Th17 cells in patients with DCM.

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Section: Introductionmentioning

confidence: 99%

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

Li¹,

Zhou²,

Tang³

et al. 2017

Cell Physiol Biochem

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“…[4][5][6][7] And thirdly, immunosuppressive therapy was shown to be associated with symptomatic and functional improvements of DCM patients in some pilot studies. 8,9) These findings jointly indicate that immune dysfunction is an important pathogenic factor of DCM.…”

mentioning

confidence: 69%

Associations Between <i>TIM1</i> Polymorphisms and Dilated Cardiomyopathy in a Han Chinese Population

Xie

Zhou

et al. 2016

Int. Heart J.

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SummaryImmune dysfunction is implicated in dilated cardiomyopathy (DCM). Previous studies found that TIM1 polymorphisms were associated with immune dysfunction. However, the associations between TIM1 polymorphisms and DCM have not been investigated. Therefore, we conducted the present study to evaluate whether TIM1 polymorphisms were associated with DCM in the Han Chinese population. A total of 396 DCM patients and 403 healthy controls were enrolled in this case-control study. Two promoter region single nucleotide polymorphisms (SNPs) of TIM1 gene, -416G>C and -1454G>A, were genotyped by PCR-RFLP. The associations between two SNPs genotyped and the overall survival (OS) of DCM patients were evaluated with Kaplan-Meier analysis and Cox regression analysis. Plasma TIM-1 levels were further measured by ELISA. We found that the C allelic frequency of -416G>C and A allelic frequency of -1454G>A were higher in DCM patients than that in controls (P < 0.001). The genotypic frequencies of both SNPs were associated with DCM susceptibility in the codominant, dominant, and overdominant models (P < 0.01). They were also associated with the OS of DCM patients in the dominant, recessive, and overdominant models (P < 0.001). The CC genotype of -416G>C and AA genotype of -1454G>A were associated with the worst prognosis (P < 0.001). In addition, the plasma TIM-1 levels in DCM patients were higher than that in controls (259.0 pg/mL versus 149.8 pg/mL, P = 0.035). The CC genotype of 416G>C and AA genotype of -1454G>A were associated with the highest TIM-1 production (P < 0.01). Overall, our findings suggest that TIM1 polymorphisms are associated with DCM susceptibility and prognosis in this Han Chinese population. (Int Heart J 2016; 57: 742-746) Key words: Single nucleotide polymorphisms, Survival analysis, Enzyme-linked immunosorbent assay D ilated cardiomyopathy (DCM), characterized by progressive ventricular chamber enlargement and contractional dysfunction in the absence of associated conditions such as hypertension, ischemic heart disease, valvular heart disease, congenital heart disease, and pulmonary heart disease, is the most common type of cardiomyopathy, accounting for approximately 55-60% of cardiomyopathies with an estimated prevalence of 1 in 2,500 individuals.1) It is the leading non-ischemic cause of congestive heart failure and sudden cardiac death, and is the most frequent indication for cardiac transplantation in adults and children. 2)In the last two decades, extensive studies have been conducted to investigate the etiology of DCM. However, the exact cause of the disease is still largely unknown. Recently, immune dysfunction was demonstrated to be involved in the pathogenesis of DCM. Firstly, it was found that T suppressor (Ts) cells are decreased while T helper (Th) cells are increased in DCM patients.3) Secondly, several cardiac-specific antibodies were detected in serum of DCM patients.4-7) And thirdly, immunosuppressive therapy was shown to be associated with symptomatic and functional improvements of DCM...

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“…A ic [6] . Autoimmunity has been proposed as a mechanism in the pathogenesis of idiopathic dilated cardiomyopathy [7] .…”

Section: Clinical Historymentioning

confidence: 99%

Multiple Sclerosis with Idiopathic Dilated Cardiomyopathy: A Case Report

Sellbach

Pender²

2005

Eur Neurol

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New insights into the pathogenesis of dilated cardiomyopathy: possible underlying autoimmune mechanisms and therapy

Cited by 43 publications

References 37 publications

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

Associations Between <i>TIM1</i> Polymorphisms and Dilated Cardiomyopathy in a Han Chinese Population

Multiple Sclerosis with Idiopathic Dilated Cardiomyopathy: A Case Report

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