Title |
Genetic ablation of Ankrd1 mitigates cardiac damage during experimental autoimmune myocarditis in mice / |
Authors |
Rinkūnaitė, Ieva ; Šimoliūnas, Egidijus ; Alksnė, Milda ; Bartkutė, Gabrielė ; Labeit, Siegfried ; Bukelskienė, Virginija ; Bogomolovas, Julius |
DOI |
10.3390/biom12121898 |
Full Text |
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Is Part of |
Biomolecules.. Basel : MDPI. 2022, vol. 12, iss. 12, art. no. 1898, p. [1-17].. eISSN 2218-273X |
Keywords [eng] |
myocarditis ; dilated cardiomyopathy ; ANKRD1 ; myocardial remodeling ; inflammation ; heart failure |
Abstract [eng] |
Myocarditis (MC) is an inflammatory disease of the myocardium that can cause sudden death in the acute phase, and dilated cardiomyopathy (DCM) with chronic heart failure as its major long-term outcome. However, the molecular mechanisms beyond the acute MC phase remain poorly understood. The ankyrin repeat domain 1 (ANKRD1) is a functionally pleiotropic stress/stretch-inducible protein, which can modulate cardiac stress response during various forms of pathological stimuli; however, its involvement in post-MC cardiac remodeling leading to DCM is not known. To address this, we induced experimental autoimmune myocarditis (EAM) in ANKRD1-deficient mice, and evaluated post-MC consequences at the DCM stage mice hearts. We demonstrated that ANKRD1 does not significantly modulate heart failure; nevertheless, the genetic ablation of Ankrd1 blunted the cardiac damage/remodeling and preserved heart function during post-MC DCM. |
Published |
Basel : MDPI |
Type |
Journal article |
Language |
English |
Publication date |
2022 |
CC license |
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