Although immune responses against group A streptococci and the heart have been correlated with antibodies and T cell responses against cardiac myosin, there is no unifying hypothesis about carditis caused globally by many different serotypes. Our study identified disease-specific epitopes of human cardiac myosin in the development of rheumatic carditis in humans. We found that immune responses to cardiac myosin were similar in rheumatic carditis among a small sample of worldwide populations, in which immunoglobulin G targeted human cardiac myosin epitopes in the S2 subfragment hinge region within S2 peptides containing amino acid residues 842-992 and 1164-1272. An analysis of rheumatic carditis in a Pacific Islander family confirmed the presence of potential rheumatogenic epitopes in the S2 region of human cardiac myosin. Our report suggests that cardiac myosin epitopes in rheumatic carditis target the S2 region of cardiac myosin and are similar among populations with rheumatic carditis worldwide, regardless of the infecting group A streptococcal M serotype.

Download full-text PDF

Source
http://dx.doi.org/10.1086/656214DOI Listing

Publication Analysis

Top Keywords

cardiac myosin
28
rheumatic carditis
20
human cardiac
12
group streptococci
8
immune responses
8
responses cardiac
8
myosin epitopes
8
cardiac
7
myosin
7
carditis
6

Similar Publications

Low-density lipoprotein receptor-related protein 6 ameliorates cardiac hypertrophy by regulating CTSD/HSP90α signaling during pressure overload.

Acta Pharmacol Sin

January 2025

Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, State Key Laboratory of Cardiovascular Diseases, NHC Key Laboratory of Ischemic Heart Diseases, and Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.

Pressure overload induces pathological cardiac remodeling, including cardiac hypertrophy and fibrosis, resulting in cardiac dysfunction or heart failure. Recently, we observed that the low-density lipoprotein receptor-related protein 6 (LRP6), has shown potential in enhancing cardiac function by mitigating cardiac fibrosis in a mouse model subjected to pressure overload. In this study, we investigated the role of LRP6 as a potential modulator of pressure overload-induced cardiac hypertrophy and elucidated the underlying molecular mechanisms.

View Article and Find Full Text PDF

Analysis of cardiac developmental toxicity induced by m-cresol in early life of zebrafish and its mechanism.

Comp Biochem Physiol C Toxicol Pharmacol

January 2025

Center for Clinical Medicine Research, First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, Jiangxi Province, China. Electronic address:

The compound m-Cresol, also referred to as 3-methylphenol,acts as a precursor in the creation of pesticides and plasticizers. This research has conducted a thorough evaluation of the toxic effects of m-cresol on the cardiac development of juvenile zebrafish, from 6 to 72 hpf. The study's results reveal that higher concentrations of m-Cresol, compared to lower ones, result in more severe heart abnormalities in zebrafish larvae.

View Article and Find Full Text PDF

Hypertrophic cardiomyopathy: insights into pathophysiology and novel therapeutic strategies from clinical studies.

Egypt Heart J

January 2025

Department of Physiology, Faculty of Basic Medical Sciences, Obafemi Awolowo College of Health Sciences, Olabisi Onabanjo University, Sagamu Campus, Sagamu, Ogun State, Nigeria.

Background: Hypertrophic cardiomyopathy (HCM) is a frequently encountered cardiac condition worldwide, often inherited, and characterized by intricate phenotypic and genetic manifestations. The natural progression of HCM is diverse, largely due to mutations in the contractile and relaxation proteins of the heart. These mutations disrupt the normal structure and functioning of the heart muscle, particularly affecting genes that encode proteins involved in the contraction and relaxation of cardiac muscle.

View Article and Find Full Text PDF

The cardiac myosin binding protein-C (cMyBP-C) regulates cross-bridge formation and controls the duration of systole and diastole at the whole heart level. As known, mutations in cMyBP-C increase the cross-bridge number and rate of their cycling, hypercontractility, and myocardial hypertrophy. We investigated the effects of the mutations D75N and P161S of cMyBP-C related to hypertrophic cardiomyopathy on the mechanism of force generation in isolated slow skeletal muscle fibers.

View Article and Find Full Text PDF

Hypertrophic cardiomyopathy (HCM) is a heterogeneous group of heart muscle disorders that affects millions, with an incidence from 1 in 500 to 1 in 200. Factors such as genetics, age, gender, comorbidities, and environmental factors may contribute to the course of this disease. Diagnosis of HCM has improved significantly in the past few decades from simple echocardiographic evaluations to a more complex, multimodal approach embracing advanced imaging, genetic, and biomarker studies.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!