Mda5

Cardiac involvement in a case of juvenile dermatomyositis with positive anti‐melanoma differentiation associated protein 5 antibody

“…Although cardiac involvement is not an expected involvement in anti‐MDA5‐positive JDM cases, it can be fatal. MDA5 has an important role in the recognition of viral ribonucleic acids 6 . In a transgenic mouse model with MDA5 overexpression, lower viral load, reduced apoptosis in cardiomyocytes, protection against viral myocarditis, and increased survival rates were demonstrated 7 .…”

“…MDA5 has an important role in the recognition of viral ribonucleic acids. 6 In a transgenic mouse model with MDA5 overexpression, lower viral load, reduced apoptosis in cardiomyocytes, protection against viral myocarditis, and increased survival rates were demonstrated. 7 It is possible that antibody formation against MDA5 in JDM may deactivate this protein, thereby increasing susceptibility to myocarditis.…”

Anti–melanoma differentiation–associated gene 5 dermatomyositis complicated by myopericarditis

“…To our knowledge, myocarditis and pericarditis, which we observed in our patient, has not been reported. MDA5 has an essential role in recognition of viral ribonucleic acids 2, 3. A transgenic mouse model with overexpression of MDA5 is protected against viral myocarditis as demonstrated by increased survival and lower viral load, cardiomyocyte apoptosis, and myocardial dysfunction 3 indicating the vital role that MDA5 plays in protection against viral myocarditis.…”

“…Depending on the dermatomyositis subtype, the myocardium can sometimes be involved 1 . Anti–melanoma differentiation–associated gene 5 (anti-MDA5) is a protein that recognizes viral particles and plays a vital role in innate immunity, 2 including protection against myocarditis 3 . MDA5 antibody–positive dermatomyositis has a unique presentation of cutaneous and mucosal ulcerations with progressive interstitial lung disease 4, 5.…”

The Role of Sex Differences in Autophagy in the Heart During Coxsackievirus B3-Induced Myocarditis

“…Our preliminary data obtained during infection with CVB3 suggest that c-FLIP S supports autophagy and therefore enhances CVB3 replication (Buskiewicz, unpublished). Furthermore, we found evidence that c-FLIP S , but not c-FLIP L , interferes with the antiviral retinoic acid inducible gene I (RIG-I) helicase signaling pathway, which was shown to protect the heart during CVB3 infection [55]. Recent evidence indicates that the autophagy related proteins Atg5-Atg12 will interfere with RIG-I pathway mediated type I interferon (IFN) signaling through direct interaction with RIG-I helicases and the mitochondrial antiviral-signaling protein (MAVS) via their caspase recruitment domains (CARD) [56].…”