Genetic Ablation of <i>Ankrd1</i> Mitigates Cardiac Damage during Experimental Autoimmune Myocarditis in Mice
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...
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MDPI AG
2022-12-01
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| Series: | Biomolecules |
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| Online Access: | https://www.mdpi.com/2218-273X/12/12/1898 |
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| author | Ieva Rinkūnaitė Egidijus Šimoliūnas Milda Alksnė Gabrielė Bartkutė Siegfried Labeit Virginija Bukelskienė Julius Bogomolovas |
| author_facet | Ieva Rinkūnaitė Egidijus Šimoliūnas Milda Alksnė Gabrielė Bartkutė Siegfried Labeit Virginija Bukelskienė Julius Bogomolovas |
| author_sort | Ieva Rinkūnaitė |
| collection | DOAJ |
| description | 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 <i>Ankrd1</i> blunted the cardiac damage/remodeling and preserved heart function during post-MC DCM. |
| first_indexed | 2024-03-09T17:16:10Z |
| format | Article |
| id | doaj.art-6488a01f4b354b5fab65615bbc7394c8 |
| institution | Directory Open Access Journal |
| issn | 2218-273X |
| language | English |
| last_indexed | 2024-03-09T17:16:10Z |
| publishDate | 2022-12-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biomolecules |
| spelling | doaj.art-6488a01f4b354b5fab65615bbc7394c82023-11-24T13:35:18ZengMDPI AGBiomolecules2218-273X2022-12-011212189810.3390/biom12121898Genetic Ablation of <i>Ankrd1</i> Mitigates Cardiac Damage during Experimental Autoimmune Myocarditis in MiceIeva Rinkūnaitė0Egidijus Šimoliūnas1Milda Alksnė2Gabrielė Bartkutė3Siegfried Labeit4Virginija Bukelskienė5Julius Bogomolovas6Department of Biological Models, Institute of Biochemistry, Life Sciences Center, Vilnius University, LT-10257 Vilnius, LithuaniaDepartment of Biological Models, Institute of Biochemistry, Life Sciences Center, Vilnius University, LT-10257 Vilnius, LithuaniaDepartment of Biological Models, Institute of Biochemistry, Life Sciences Center, Vilnius University, LT-10257 Vilnius, LithuaniaDepartment of Biological Models, Institute of Biochemistry, Life Sciences Center, Vilnius University, LT-10257 Vilnius, LithuaniaDZHK Partner Site Mannheim-Heidelberg, Medical Faculty Mannheim, University of Heidelberg, 68167 Mannheim, GermanyDepartment of Biological Models, Institute of Biochemistry, Life Sciences Center, Vilnius University, LT-10257 Vilnius, LithuaniaDepartment of Medicine, School of Medicine, University of California, San Diego (UCSD), La Jolla, CA 92093, USAMyocarditis (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 <i>Ankrd1</i> blunted the cardiac damage/remodeling and preserved heart function during post-MC DCM.https://www.mdpi.com/2218-273X/12/12/1898myocarditisdilated cardiomyopathyANKRD1myocardial remodelinginflammationheart failure |
| spellingShingle | Ieva Rinkūnaitė Egidijus Šimoliūnas Milda Alksnė Gabrielė Bartkutė Siegfried Labeit Virginija Bukelskienė Julius Bogomolovas Genetic Ablation of <i>Ankrd1</i> Mitigates Cardiac Damage during Experimental Autoimmune Myocarditis in Mice Biomolecules myocarditis dilated cardiomyopathy ANKRD1 myocardial remodeling inflammation heart failure |
| title | Genetic Ablation of <i>Ankrd1</i> Mitigates Cardiac Damage during Experimental Autoimmune Myocarditis in Mice |
| title_full | Genetic Ablation of <i>Ankrd1</i> Mitigates Cardiac Damage during Experimental Autoimmune Myocarditis in Mice |
| title_fullStr | Genetic Ablation of <i>Ankrd1</i> Mitigates Cardiac Damage during Experimental Autoimmune Myocarditis in Mice |
| title_full_unstemmed | Genetic Ablation of <i>Ankrd1</i> Mitigates Cardiac Damage during Experimental Autoimmune Myocarditis in Mice |
| title_short | Genetic Ablation of <i>Ankrd1</i> Mitigates Cardiac Damage during Experimental Autoimmune Myocarditis in Mice |
| title_sort | genetic ablation of i ankrd1 i mitigates cardiac damage during experimental autoimmune myocarditis in mice |
| topic | myocarditis dilated cardiomyopathy ANKRD1 myocardial remodeling inflammation heart failure |
| url | https://www.mdpi.com/2218-273X/12/12/1898 |
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