2020
DOI: 10.1111/jcmm.15913
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Deficit of glucocorticoid‐induced leucine zipper amplifies angiotensin‐induced cardiomyocyte hypertrophy and diastolic dysfunction

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Cited by 7 publications
(2 citation statements)
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“…Moreover, GILZ involvement in cardiovascular diseases was very recently observed in an angiotensin-induced model of hypertrophy and diastolic disfunction in mice. In that experimental model, GILZ-KO mice showed enhanced cardiomyocyte hypertrophy with normal myocardial inflammatory and fibrotic reaction, suggesting that GILZ is involved in hypertrophic growth but not in local inflammation [ 96 ]. Furthermore, in a mouse model of heart infarction, reduced cardiac GILZ correlated with strong immune and inflammatory responses, whereas intramyocardial GILZ delivery increased Tregs and IL-10+ cells, while reducing Th-17 lymphocytes with subsequent cardioprotection [ 68 ].…”
Section: Gilz In Various Cell Typesmentioning
confidence: 99%
“…Moreover, GILZ involvement in cardiovascular diseases was very recently observed in an angiotensin-induced model of hypertrophy and diastolic disfunction in mice. In that experimental model, GILZ-KO mice showed enhanced cardiomyocyte hypertrophy with normal myocardial inflammatory and fibrotic reaction, suggesting that GILZ is involved in hypertrophic growth but not in local inflammation [ 96 ]. Furthermore, in a mouse model of heart infarction, reduced cardiac GILZ correlated with strong immune and inflammatory responses, whereas intramyocardial GILZ delivery increased Tregs and IL-10+ cells, while reducing Th-17 lymphocytes with subsequent cardioprotection [ 68 ].…”
Section: Gilz In Various Cell Typesmentioning
confidence: 99%
“…Mechanistically, this study suggests that GILZ may interact with FoxP3 and GATA4 in the development of cardiac hypertrophy. FoxP3 and GATA4 were markedly upregulated after Ang II, but in the hearts of GILZ-knockout mice, such an increase was less pronounced (for FoxP3) or absent (for GATA4) [94]. Although the details of molecular interplay of GILZ with FoxP3 or GATA4 in cardiomyocytes remain to be determined, the absence of GILZ may condition their expression, leading to the excessive hypertrophic response.…”
Section: Myocardial Damage and Remodelingmentioning
confidence: 96%