Key result
Ankrd1 ablation blunts cardiac remodeling and preserves heart function in mice with post-myocarditis DCM.
Why the study?
Molecular mechanisms beyond acute myocarditis leading to dilated cardiomyopathy remain poorly understood, and the involvement of ANKRD1 in post-myocarditis cardiac remodeling is unknown.
Does genetic ablation of Ankrd1 mitigate cardiac damage in mice with experimental autoimmune myocarditis?
Does genetic ablation of Ankrd1 mitigate cardiac damage in mice with experimental autoimmune myocarditis?
Genetic ablation of Ankrd1 in a mouse model mitigates cardiac damage and preserves heart function following experimental autoimmune myocarditis.
Hypothesis-generating for Ankrd1 targeting in myocarditis; leaves open translation to human dilated cardiomyopathy.
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.
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Rinkūnaitė et al. (2022) studied Experimental autoimmune myocarditis. Genetic ablation of Ankrd1 was evaluated on Cardiac damage/remodeling and heart function. Genetic ablation of Ankrd1 blunted cardiac damage and remodeling and preserved heart function during post-myocarditis dilated cardiomyopathy in mice.
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