Cellular Immunology of Myocarditis: Lights and Shades—A Literature Review DOI Creative Commons
Cristina Vicenzetto, Andrea Silvio Giordani, Caterina Menghi

et al.

Cells, Journal Year: 2024, Volume and Issue: 13(24), P. 2082 - 2082

Published: Dec. 17, 2024

Myocarditis is an inflammatory disease of the myocardium with heterogeneous etiology, clinical presentation, and prognosis; when it associated myocardial dysfunction, this identifies entity cardiomyopathy. In last few decades, relevance immune system in myocarditis onset progression has become evident, thus having crucial terms treatment prognostic stratification. fact, advances cardiac immunology have led to a better characterization cellular subtypes involved pathogenesis cardiomyopathy, whether etiology infectious or autoimmune/immune-mediated. The difference course between spontaneous recovery acute, subacute, chronic end-stage heart failure may be explained not only by classical markers but also through immune-pathological mechanisms at level. Nevertheless, much still needs clarified molecular especially biopsy-proven myocarditis. aims review are (1) describe cardiomyopathy immune-mediated/autoimmune forms, (2) analyze recent findings on role different cells myocarditis, (3) illustrate potential such findings, (4) highlight need further studies pivotal areas immunology.

Language: Английский

NaV1.5 autoantibodies in Brugada syndrome: pathogenetic implications DOI Creative Commons
Adriana Tarantino, Giuseppe Ciconte, Dario Melgari

et al.

European Heart Journal, Journal Year: 2024, Volume and Issue: 45(40), P. 4336 - 4348

Published: July 30, 2024

Abstract Background and Aims Patients suffering from Brugada syndrome (BrS) are predisposed to life-threatening cardiac arrhythmias. Diagnosis is challenging due the elusive electrocardiographic (ECG) signature that often requires unconventional ECG lead placement drug challenges be detected. Although NaV1.5 sodium channel dysfunction a recognized pathophysiological mechanism in BrS, only 25% of patients have detectable SCN5A variants. Given emerging role autoimmunity ion function, this study explores presence potential impact anti-NaV1.5 autoantibodies BrS patients. Methods Using engineered HEK293A cells expressing recombinant protein, plasma 50 controls was screened for via western blot, with specificity confirmed by immunoprecipitation immunofluorescence. The these on current density their effects were assessed cellular models through injection wild-type mice. Results Anti-NaV1.5 detected 90% vs. 6% controls, yielding diagnostic area under curve .92, 94% sensitivity. These findings consistent across varying patient demographics independent mutation status. Electrophysiological studies demonstrated significant reduction specifically density. Notably, mice injected showed Brugada-like abnormalities, supporting pathogenic autoantibodies. Conclusions demonstrates majority patients, suggesting an immunopathogenic component beyond genetic predispositions. autoantibodies, which could serve as additional markers, also prompt reconsideration underlying mechanisms evidenced inducing encourage more comprehensive approach point new avenues therapeutic research.

Language: Английский

Citations

6
Viral Infection and Connexin Dysfunction in the Heart DOI Creative Commons
Chelsea M. Phillips, James W. Smyth

Current Cardiology Reports, Journal Year: 2025, Volume and Issue: 27(1)

Published: March 27, 2025

Abstract Purpose of review Gap junctions, comprising connexin proteins, enable the direct intercellular electrical coupling cardiomyocytes, and disruption this process is arrhythmogenic. In addition, gap junctions effect metabolic relevance to review, propagate host antiviral immune responses. Accordingly, connexins have emerged as viral targets during infection. This summarizes current knowledge regarding contributions inflammation vs virally encoded factors in driving alterations cardiac junction function. Recent findings addition immune-mediated effects on electrophysiology myocarditis, there now increasing appreciation for targeting function acute/active Summary We know diverse species independently evolved directly target Understanding both indirect infection critical inform treatment strategies development novel therapeutics acute a distinct disease from chronic myocarditis.

Language: Английский

Citations

0
Emerging concepts in inflammatory cardiomyopathy DOI
Nisha A. Gilotra, Enrico Ammirati

International Journal of Cardiology, Journal Year: 2024, Volume and Issue: 406, P. 132058 - 132058

Published: April 16, 2024

Language: Английский

Citations

1
Myocarditis and Arrhythmias DOI
Antonio Abbate, Pietro Enea Lazzerini

JACC. Clinical electrophysiology, Journal Year: 2024, Volume and Issue: 10(6), P. 1175 - 1177

Published: May 15, 2024

Language: Английский

Citations

1
Macrophage-derived VEGF-C reduces cardiac inflammation and prevents heart dysfunction in CVB3-induced viral myocarditis via remodeling cardiac lymphatic vessels DOI

Yi-Lian Chen,

Yuan-Nan Lin,

Jing Xu

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 143, P. 113377 - 113377

Published: Oct. 14, 2024

Language: Английский

Citations

0
Cellular Immunology of Myocarditis: Lights and Shades—A Literature Review DOI Creative Commons
Cristina Vicenzetto, Andrea Silvio Giordani, Caterina Menghi

et al.

Cells, Journal Year: 2024, Volume and Issue: 13(24), P. 2082 - 2082

Published: Dec. 17, 2024

Myocarditis is an inflammatory disease of the myocardium with heterogeneous etiology, clinical presentation, and prognosis; when it associated myocardial dysfunction, this identifies entity cardiomyopathy. In last few decades, relevance immune system in myocarditis onset progression has become evident, thus having crucial terms treatment prognostic stratification. fact, advances cardiac immunology have led to a better characterization cellular subtypes involved pathogenesis cardiomyopathy, whether etiology infectious or autoimmune/immune-mediated. The difference course between spontaneous recovery acute, subacute, chronic end-stage heart failure may be explained not only by classical markers but also through immune-pathological mechanisms at level. Nevertheless, much still needs clarified molecular especially biopsy-proven myocarditis. aims review are (1) describe cardiomyopathy immune-mediated/autoimmune forms, (2) analyze recent findings on role different cells myocarditis, (3) illustrate potential such findings, (4) highlight need further studies pivotal areas immunology.

Language: Английский

Citations

0