Potential role of antibodies against cardiac Kv channel-interacting protein 2 in dilated cardiomyopathy

Landsberger, Martin; Staudt, Alexander; Choudhury, Sangita; Trimpert, Christiane; Herda, Lars R.; Klingel, Karin; Kandolf, Reinhard; Schultheiss, Heinz‐Peter; Kroemer, Heyo K.; Völker, Uwe; Felix, Stephan B.

doi:10.1016/j.ahj.2008.02.015

Cited by 27 publications

(26 citation statements)

References 32 publications

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“…Most studies assessed anti-troponin I antibodies (9,12,14,(39)(40)(41)(42)(45)(46)(47)(48)50,51,(53)(54)(55)(56)(57)(58), whereas anti-troponin T antibodies were assessed in only 16% (n=1,636) of individuals (11,43,44,49,52) (including 993 individuals where both types of autoantibodies were evaluated) (11,44,49).…”

Section: Resultsmentioning

confidence: 99%

“…Only one study presented data concerning anti-troponin T autoantibodies in DCM (11). Importantly, a total of 3,661 healthy (or presumably healthy) individuals were also assessed, though mainly as control groups (9,11,14,39,40,(43)(44)(45)(46)(47)(48)(49)52,54,56,58).…”

Section: Resultsmentioning

confidence: 99%

“…Over half of the studies included assessed individuals with cardiovascular diseases (9,11,12,14,39,40,(44)(45)(46)(47)(48)50,51,53,(55)(56)(57), especially DCM. The prevalence of anti-troponin I autoantibodies in DCM ranged from 7.0% (11) to 22.2% (in patients prior to immunoadsorption, notably decreased to 3.7% after immunoadsorption) (53).…”

Section: Resultsmentioning

confidence: 99%

“…Research has shown that autoantibodies against different cardiac antigens (such as beta-1 adrenoceptors) can have an important role in the pathophysiology of heart diseases, namely HF (4,56). In a recent study in the setting of ST-elevation acute MI, beta-1 adrenoceptor autoantibodies were associated with adverse outcomes (being an independent predictor of major adverse cardiovascular events) (39).…”

Section: Discussionmentioning

confidence: 99%

“…were included in the quantitative synthesis ( Table 2) (9,11,14,40,45,(47)(48)(49)52,56,58). The prevalence of antitroponin antibodies in healthy individuals ranged from 0.0% to 20.0% for anti-troponin I (9,11,14,45,47,58) and from 0.0% to 9.9% for anti-troponin T (11,49,52).…”

Section: Page 4 Of 16mentioning

confidence: 99%

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Anti-cardiac troponin antibodies in clinical human disease: a systematic review

Vilela¹,

Bettencourt‐Silva²,

Costa³

et al. 2017

Ann. Transl. Med.

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Anti-cardiac troponin antibodies have been studied in different types of clinical diseases and in healthy populations. A systematic review of published data on anti-troponin antibodies was carried out (search performed on PubMed, ISI Web of Knowledge and Scopus databases). From title and abstract analysis, thirty-three articles were included that met the pre-specified criteria; after full-text analysis, nine articles were excluded. Most studies assessed anti-troponin I antibodies. The prevalence of anti-cardiac troponin antibodies in healthy individuals ranged from 0.0% to 20.0%. The prevalence of anti-troponin I autoantibodies in dilated cardiomyopathy (DCM) ranged from 7.0% to 22.2%. Other conditions under study were myocardial infarction, ischemic cardiomyopathy (ICM), peripartum cardiomyopathy (PPCM), Chagas disease, Emery-Dreifuss muscular dystrophy (EDMD) and renal transplantation. In the different patient populations studied, anti-cardiac troponin antibodies have been shown to be either positively or negatively associated with prognostic and clinical features. In what concerns a possible value as biomarkers, these assays have not emerged up to the present moment as important aids for practical clinical decisions in cardiac or other types of patients. In what concerns pathophysiology, anti-cardiac troponin autoantibodies may play a role in different diseases. It can be speculated that these antibodies could be involved in perpetuating some degree of cardiac injury after an event, such as myocardial infarction or PPCM. The major function of the heart is its contractile function, and cardiac muscle contains sarcomeres, which include different types of molecules, of which actin and myosin are essential for strength generation during contraction. Other molecules, such as cardiac troponins, play a role of regulation concerning cardiac muscle contraction. Cardiac troponins I and T have been shown to be different molecules than the corresponding ones in skeletal muscle, and have gained importance as cardiac biomarkers (1,2).Research has shown that antibodies against cardiac troponins exist in different settings, and questions about their role in the cardiovascular pathological continuum have emerged over the last years. The possible role of cardiac troponin autoantibodies in disease processes [and particularly in dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM)] has gained interest (3-6).Animal models in mice have demonstrated that anticardiac troponin I autoantibodies are capable of inducing heart dilatation and dysfunction, apparently through interactions with the calcium balance in cardiomyocytes (7). Okazaki et al. showed that in mice antibodies to cardiac troponin I stained the surface of cardiomyocytes, implying the presence of troponin I on the cell surface (differing from cardiac troponin T) (7). Göser et al. immunized mice with cardiac troponin I, leading to severe inflammation of the myocardium, cardiomegaly, fibrosis and 30% mortality over 270 days (8). However, in a study carri...

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Page 4 Of 16mentioning

confidence: 99%

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Anti-cardiac troponin antibodies in clinical human disease: a systematic review

Vilela¹,

Bettencourt‐Silva²,

Costa³

et al. 2017

Ann. Transl. Med.

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The role of B cells in heart failure and implications for future immunomodulatory treatment strategies

et al. 2020

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Despite numerous demonstrations that the immune system is activated in heart failure, negatively affecting patients' outcomes, no definitive treatment strategy exists directed to modulate the immune system. In this review, we present the evidence that B cells contribute to the development of hypertrophy, inflammation, and maladaptive tissue remodelling. B cells produce antibodies that interfere with cardiomyocyte function, which culminates as the result of recruitment and activation of a variety of innate and structural cell populations, including neutrophils, macrophages, fibroblasts, and T cells. As B cells appear as active players in heart failure, we propose here novel immunomodulatory therapeutic strategies that target B cells and their products.

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Antibodies Against Potassium Channel Interacting Protein 2 Induce Necrosis in Isolated Rat Cardiomyocytes

et al. 2014

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Auto-antibodies against cardiac proteins have been described in patients with dilated cardiomyopathy. Antibodies against the C-terminal part of KChIP2 (anti-KChIP2 [C-12]) enhance cell death of rat cardiomyocytes. The underlying mechanisms are not fully understood. Therefore, we wanted to explore the mechanisms responsible for anti-KChIP2-mediated cell death. Rat cardiomyocytes were treated with anti-KChIP2 (C-12). KChIP2 RNA and protein expressions, nuclear NF-κB, mitochondrial membrane potential Δψm, caspase-3 and -9 activities, necrotic and apoptotic cells, total Ca(2+) and K(+) concentrations, and the effects on L-type Ca(2+) channels were quantified. Anti-KChIP2 (C-12) induced nuclear translocation of NF-κB. Anti-KChIP2 (C-12)-treatment for 2 h significantly reduced KChIP2 mRNA and protein expression. Anti-KChIP2 (C-12) induced nuclear translocation of NF-κB after 1 h. After 6 h, Δψm and caspase-3 and -9 activities were not significantly changed. After 24 h, anti-KChIP2 (C-12)-treated cells were 75 ± 3% necrotic, 2 ± 1% apoptotic, and 13 ± 2% viable. Eighty-six ± 1% of experimental buffer-treated cells were viable. Anti-KChIP2 (C-12) induced significant increases in total Ca(2+) (plus 11 ± 2%) and K(+) (plus 18 ± 2%) concentrations after 5 min. Anti-KChIP2 (C-12) resulted in an increased Ca(2+) influx through L-type Ca(2+) channels. In conclusion, our results suggest that anti-KChIP2 (C-12) enhances cell death of rat cardiomyocytes probably due to necrosis.

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Potential role of antibodies against cardiac Kv channel-interacting protein 2 in dilated cardiomyopathy

Cited by 27 publications

References 32 publications

Anti-cardiac troponin antibodies in clinical human disease: a systematic review

Anti-cardiac troponin antibodies in clinical human disease: a systematic review

The role of B cells in heart failure and implications for future immunomodulatory treatment strategies

Antibodies Against Potassium Channel Interacting Protein 2 Induce Necrosis in Isolated Rat Cardiomyocytes

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