CD69 Limits the Severity of Cardiomyopathy After Autoimmune Myocarditis | Zendy

Aránzazu CruzAdalia | Zendy; Luis Jesús JiménezBorreguero | Zendy; Marta RamírezHuesca | Zendy; Isabel ChicoCalero | Zendy; Olga Barreiro | Zendy; Erica López-Conesa | Zendy; Manuel Fresno | Zendy; Francisco SánchezMadrid | Zendy; Pilar Martı́n | Zendy

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CD69 Limits the Severity of Cardiomyopathy After Autoimmune Myocarditis

Author(s) -

Aránzazu CruzAdalia,

Luis Jesús JiménezBorreguero,

Marta RamírezHuesca,

Isabel ChicoCalero,

Olga Barreiro,

Erica López-Conesa,

Manuel Fresno,

Francisco SánchezMadrid,

Pilar Martı́n

Publication year - 2010

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.110.952820

Subject(s) - medicine , myocarditis , cardiomyopathy , heart failure , inflammation , fibrosis , dilated cardiomyopathy , ejection fraction , myocardial fibrosis , edema , adoptive cell transfer , cardiology , pathology , immunology , immune system , t cell

Experimental autoimmune myocarditis (EAM), a mouse model of post-infectious cardiomyopathy, reflects mechanisms of inflammatory cardiomyopathy in humans. EAM is characterized by an infiltration of inflammatory cells into the myocardium that can be followed by myocyte fibrosis, edema, and necrosis, leading to ventricular wall dysfunction and heart failure. Different data indicate that CD69 exerts an important immunoregulatory effect in vivo. However, the possible role of CD69 in autoimmune myocarditis has not been studied.

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