| Title |
Miokardito ir dilatacinės kardiomiopatijos molekulinių mechanizmų tyrimai |
| Translation of Title |
Study of molecular mechanisms of myocarditis and dilated cardiomyopathy. |
| Authors |
Rinkūnaitė, Ieva |
| DOI |
10.15388/vu.thesis.474 |
| Full Text |
|
| Pages |
232 |
| Keywords [eng] |
myocarditis ; dilated cardiomyopathy ; parvovirus B19 ; VP1u ; ANKRD1 |
| Abstract [eng] |
Heart failure is a significant and growing public health problem worldwide that poses many challenges due to the vast diversity of etiologic factors. Myocarditis and dilated cardiomyopathy are among the leading causes of heart failure. Gaining new insights into the causal pathophysiological mechanisms of these diseases would contribute to developing of more effective prevention and treatment strategies for heart failure. This dissertation investigated the possible molecular pathophysiological mechanisms underlying myocarditis and dilated cardiomyopathy associated with parvovirus B19 and ANKRD1 protein. Our in vitro study demonstrates the unique region of the parvovirus B19 capsid protein VP1 cannot be considered the sole determinant of cell and species tropism of parvovirus B19. Furthermore, exposure to the unique region of VP1 leads to activation and stress response of primary endothelial cells, irrespective of its internalization potential. This novel mechanism may contribute to the pathophysiology of parvovirus B19-associated myocarditis. In vivo studies revealed that ANKRD1 protein does not play a major role during murine post-myocarditis cardiac remodeling leading to dilated cardiomyopathy. However, the genetic ablation of Ankrd1 mitigates cardiac tissue damage and remodeling. These findings suggest that timely pharmacological regulation of ANKRD1 expression could be a potential target for mitigating the outcome of myocarditis-induced DCM. |
| Type |
Doctoral thesis |
| Language |
Lithuanian |
| Publication date |
2023 |
