心臓血管科学者が、機能不全に陥った心臓の新たな治療法の可能性を発見(Virginia Tech cardiovascular scientist identifies potential new treatment for failing hearts)

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2024-10-28 バージニア工科大学(VirginiaTech)

バージニア工科大学の研究者ジュンコ・ウォーレンは、収縮性心不全の新たな治療法として、心臓と骨格筋で見つかるタンパク質PERM1が心筋のエネルギー生産と収縮機能を改善する可能性を示した。健康なマウスの心臓にこのタンパク質を注入した結果、ミトコンドリアの機能と収縮力が向上。今後、PERM1が同様に機能不全の心臓でも効果を発揮するか検証する予定で、心筋の強化とエネルギー代謝改善の両面から治療の可能性が期待される。

<関連情報>

アデノ随伴ウイルスによるPerm1の遺伝子導入がマウスの心収縮力を高める Adeno-associated virus-mediated gene delivery of Perm1 enhances cardiac contractility in mice

Karthi Sreedevi,Alexey V. Zaitsev,…
Heart and Circulatory Physiology  Published:7 October 2024
DOI:https://doi.org/10.1152/ajpheart.00545.2024

Abstract

Reduced muscle contractility and mitochondrial bioenergetics are the hallmarks of systolic heart failure. There is currently no therapy targeting both. Here, we show that gene delivery of Perm1 via adeno-associated virus (AAV) simultaneously enhances cardiac contractility and mitochondrial biogenesis in C57BL6 mice. Moreover, we found that PERM1 interacts with troponin C (TnC), a key contractile protein in striated muscle, and that AAV-Perm1 led to the upregulation of TnC. This study suggests that gene delivery of Perm1 may be a novel therapeutic approach to treat systolic heart failure by simultaneously restoring cardiac contractility and mitochondrial bioenergetics.

NEW & NOTEWORTHY Perm1 gene delivered with AAV9 enhances cardiac contractility in mice, and it is concomitant with the increase of mitochondrial bioenergetics and upregulation of TnC. This is the first study showing that PERM1, previously known as a striated muscle-specific mitochondrial regulator, also positively regulates cardiac contractility.

医療・健康
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