Myocarditis: causes, mechanisms, and evolving therapies

Kyaw, Tin; Drummond, Grant R; Bobik, Alex; Peter, Karlheinz

doi:10.1080/14728222.2023.2193330

Cited by 5 publications

(6 citation statements)

References 160 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…AM accounts for most cases of myocarditis (65%), although the underlying cause often cannot be identified (50%) [5]. It is mainly caused by viral disease (direct cytopathic effects of cardiotropic viruses and virusinduced anticardiac immune response) and less commonly by non-infectious etiologies [8].…”

Section: Discussionmentioning

confidence: 99%

Clinically Suspected Acute Myocarditis in the First Trimester of Twin Gestation: A Case Report

Flores-Sanga,

Salas-Cuadros,

Saucedo-Chinchay

et al. 2023

Cureus

View full text Add to dashboard Cite

Acute myocarditis (AM) in early pregnancy is a rare disease. Its clinical presentation varies from asymptomatic disease to cardiogenic shock and death. A 28-year-old woman, 12 weeks primigravida of a dichorionic and diamniotic pregnancy, was admitted for hyperemesis gravidarum, associated with a common cold-like condition. During hospitalization, she developed new-onset sinus tachycardia and dyspnea. An electrocardiogram revealed sinus tachycardia and diffuse ST-segment elevation. Laboratory tests showed elevated levels of troponin and pro-B-type natriuretic peptide. Pelvic obstetric ultrasound and chest X-ray were normal. Speckle-tracking echocardiography showed mild apical hypokinesia with preserved left ventricular ejection fraction. In view of these findings, AM was suspected, and cardiac magnetic resonance imaging was highly suggestive of AM. The patient had a favorable recovery without cardiovascular or obstetric complications.

show abstract

Section: Discussionmentioning

confidence: 99%

Clinically Suspected Acute Myocarditis in the First Trimester of Twin Gestation: A Case Report

Flores-Sanga,

Salas-Cuadros,

Saucedo-Chinchay

et al. 2023

Cureus

View full text Add to dashboard Cite

show abstract

“…The pathogenesis of myocarditis is not yet fully understood, and autoimmune mechanisms play a significant role in its development. [ 89 ] Studies have shown that the proportion of Tregs is negatively correlated with disease severity in experimental autoimmune myocarditis. [ 90 ] In addition, coxsackievirus B3 promoted Treg apoptosis in an experimental myocarditis model.…”

Section: Tregs and Progression Of Specific Cvdsmentioning

confidence: 99%

“…[ 93 ] In addition, Tregs can alleviate myocarditis and mitigate myocardial damage by facilitating the differentiation of monocytes into an anti-inflammatory phenotype. [ 89 ] Transferring virus-induced Tregs during the early stage of myocarditis can prevent myocardial fibrosis. [ 94 ] Th17/Treg imbalance can exacerbate autoimmune myocarditis.…”

Section: Tregs and Progression Of Specific Cvdsmentioning

confidence: 99%

Regulatory T cells and cardiovascular diseases

Hu,

Li,

Cheng

2023

Chinese Medical Journal

View full text Add to dashboard Cite

Inflammation is a major underlying mechanism in the progression of numerous cardiovascular diseases (CVDs). Regulatory T cells (Tregs) are typical immune regulatory cells with recognized immunosuppressive properties. Despite the immunosuppressive properties, researchers have acknowledged the significance of Tregs in maintaining tissue homeostasis and facilitating repair/regeneration. Previous studies unveiled the heterogeneity of Tregs in the heart and aorta, which expanded in CVDs with unique transcriptional phenotypes and reparative/regenerative function. This review briefly summarizes the functional principles of Tregs, also including the synergistic effect of Tregs and other immune cells in CVDs. We discriminate the roles and therapeutic potential of Tregs in CVDs such as atherosclerosis, hypertension, abdominal arterial aneurysm, pulmonary arterial hypertension, Kawasaki disease, myocarditis, myocardial infarction, and heart failure. Tregs not only exert anti-inflammatory effects but also actively promote myocardial regeneration and vascular repair, maintaining the stability of the local microenvironment. Given that the specific mechanism of Tregs functioning in CVDs remains unclear, we reviewed previous clinical and basic studies and the latest findings on the function and mechanism of Tregs in CVDs.

show abstract

“…Recently, VMC has been of renewed interest due to a dramatic increase in the number of patients with VMC as a result of a widespread epidemic of a new coronavirus. 2 , 7 , 8 Previous studies have confirmed that there are many known and unknown causes of DCM, the known causes of DCM are mainly infection, genetic, and immune factors, viral infection is an important factor causing DCM, and the most common in temperate regions is Coxsackie B virus. There are many types of DCM, including idiopathic DCM, viral DCM, and familial DCM.…”

Section: Introductionmentioning

confidence: 99%

“…Viral myocarditis (VMC), characterized by degeneration and necrosis of cardiac myocytes, is an inflammatory myocardial lesion caused by the invasion of the heart by viruses, especially Coxsackie B group. 1 , 2 After the acute phase of VMC, the virus persists as a molecular pathogen potentially in the myocardial tissue, causing persistent myocardial damage and leading to myocardial degeneration, microvascular dysfunction, and myocardial cell fibrosis. In a large number of cases, the above lesions cause myocardial hypertrophy, enlargement of the heart chambers, abnormal cardiac function, and eventually dilated cardiomyopathy (DCM).…”

Section: Introductionmentioning

confidence: 99%

Identification of the communal pathogenesis and immune landscape between viral myocarditis and dilated cardiomyopathy

Lei,

Cao,

et al. 2023

ESC Heart Failure

View full text Add to dashboard Cite

AimsStudies have confirmed that viral myocarditis (VMC) is one of the risk factors for dilated cardiomyopathy (DCM). The molecular mechanisms underlying the progression from VMC to DCM remain unclear and require further investigation.Methods and resultsThe mRNA microarray datasets GSE57338 (DCM) and GSE1145 (VMC) were obtained from the Gene Expression Omnibus database. The candidate key genes were further screened using weighted correlation network analysis (WGCNA), protein–protein interaction and external dataset validation, and the correlation between the candidate key genes and immune cells and the signalling pathways of the candidate key genes were observed by enrichment analysis and immune infiltration analysis. The expression of key genes was validated in the external dataset GSE35182. The crosstalk genes between DCM and VMC were mainly enriched in ‘transcriptional misregulation in cancer’, ‘FoxO signalling pathway’, ‘AGE‐RAGE signalling pathway in diabetic complications’, ‘thyroid hormone signalling pathway’, ‘AMPK signalling pathway’, and other signalling pathways. The immune infiltration analysis indicated that VMC was mainly associated with resting dendritic cells and M0 macrophages, while DCM was mainly associated with monocytes, M0 macrophages, CD8+ T cells, resting CD4 memory T cells, naive CD4+ T cells, and resting mast cells. In DCM‐related dataset GSE57338 and VMC‐related dataset GSE1145, a total of 18 candidate key genes were differentially expressed. BLC6, FOXO1, and UBE2M were identified as the key genes that lead to the progression from VMC to DCM by GSE35182.ConclusionsThree key genes (BLC6, FOXO1, and UBE2M) were identified and provided new insights into the diagnosis and treatment of VMC with DCM.

show abstract

Myocarditis: causes, mechanisms, and evolving therapies

Cited by 5 publications

References 160 publications

Clinically Suspected Acute Myocarditis in the First Trimester of Twin Gestation: A Case Report

Clinically Suspected Acute Myocarditis in the First Trimester of Twin Gestation: A Case Report

Regulatory T cells and cardiovascular diseases

Identification of the communal pathogenesis and immune landscape between viral myocarditis and dilated cardiomyopathy

Contact Info

Product

Resources

About