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Updated: Feb 25, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

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ヒストンメチルトランスフェラーゼG9aは,心筋細胞ホメオスタシスおよび高縮のために必要である

Roberto Papait1, Simone Serio2, Christina Pagiatakis2

  • 1From Department of Cardiovascular Medicine, Humanitas Research Hospital, Rozzano, Milan, Italy (R.P., S.S., C.P., F.R., P.C., N.S., M. Miragoli, G.C.); Genetic and Biomedical Research Institute, National Research Council of Italy, Rozzano, Milan, Italy (R.P., F.R., P.C., N.S., G.C.); Humanitas University, Rozzano, Milan, Italy (M. Mazzola, G.C.); School of Medicine, University of Verona, Italy (M. Mazzola); and Department of Medicine and Surgery, University of Parma, Italy (M. Miragoli). roberto.papait@humanitasresearch.it gianluigi.condorelli@hunimed.eu.

Circulation
|August 6, 2017
PubMed
まとめ

ヒストンメチルトランスフェラーゼG9aは,心筋細胞ホメオスタシスを維持し,心筋縮を促進する遺伝子を抑制することによって,成人の心臓機能に不可欠です. このエピジェネティック・レギュレータは 心臓病の治療対象となる可能性があります

キーワード:
EHMT2タンパク質 マウスマウスのMEF2Cタンパク質エピゲノミクス心不全ヘテロクロマチンヒストンのメチル化ハイパートロフィー

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