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Article Synopsis
  • Growth differentiation factor 11 (GDF11) plays a crucial role in various animal tissues and is linked to several therapeutic effects, including anti-aging and anti-tumor benefits.
  • * Recent interest from both academic and commercial sectors has emerged, with ongoing developments in GDF11-based therapeutics, notably the antibody drug Sotatercept that is nearing marketing approval.
  • * This review emphasizes the need for comprehensive research on GDF11's functions, its cellular interactions, and current challenges to enhance understanding and treatment strategies moving forward.
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A wide range of anti-myocardial autoantibodies have been reported since the 1970s. Among them, autoantibodies against the β-adrenergic receptor (βAR-AAb) have been the most thoroughly investigated, especially in dilated cardiomyopathy (DCM). ΒAR-Aabs have agonist effects inducing desensitization of βAR, cardiomyocyte apoptosis, and sustained calcium influx which lead to cardiac dysfunction and arrhythmias.

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Background: Familial hypercholesterolemia (FH) can lead to premature coronary heart disease. Anticardiolipin antibody may be a contributor for thrombosis. Here, we report an adult with possible FH suffered from premature myocardial infarction that may be triggered by transient increased anticardiolipin antibody.

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Objective: Myasthenia gravis (MG) is an immunological disorder of the neuromuscular junction, characterized by easy fatigability and weakness of the skeletal muscles. However, it has sometimes been reported that heart diseases including cardiomyopathies leading to sudden death have been observed in patients with MG. We studied the prevalence of electrocardiographic (ECG) abnormalities and heart disease in patients newly diagnosed with MG who had not received immunotherapy.

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Although genetic abnormalities play a pivotal role in the development of dilated cardiomyopathy (DCM), acquired infection and autoimmune abnormalities, or both, appear to be predominant underlying disorders. Of these, viral infection causes target organ damage via perforin produced by suppressor T cells. Thereafter, various antigens released from damaged myocytes are presented on the major histocompatibility complex II, which is expressed in antigen-presenting cells, resulting in activation of both cellular (Th1) and humoral (Th2) immunity.

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