学術雑誌論文

学術雑誌論文

Cell Reports. 2024, 43(12), p. 115001

AMPK regulates Bcl2-L-13-mediated mitophagy induction for cardioprotection

Elsevier B.V.

英語

2024-12-24

https://doi.org/10.1016/j.celrep.2024.115001

Murakawa T., Ito J., Rusu M.C., et al. AMPK regulates Bcl2-L-13-mediated mitophagy induction for cardioprotection. Cell Reports 43, 115001 (2024); https://doi.org/10.1016/j.celrep.2024.115001.

The accumulation of damaged mitochondria in the heart is associated with heart failure. Mitophagy is an autophagic degradation system that specifically targets damaged mitochondria. We have reported previously that Bcl2-like protein 13 (Bcl2-L-13) mediates mitophagy and mitochondrial fission in mammalian cells. However, the in vivo function of Bcl2-L-13 remains unclear. Here, we demonstrate that Bcl2-L-13-deficient mice and knockin mice, in which the phosphorylation site (Ser272) on Bcl2-L-13 was changed to Ala, showed left ventricular dysfunction in response to pressure overload. Attenuation of mitochondrial fission and mitophagy led to impairment of ATP production in these mouse hearts. In addition, we identified AMPKα2 as the kinase responsible for the phosphorylation of Bcl2-L-13 at Ser272. These results indicate that Bcl2-L-13 and its phosphorylation play an important role in maintaining cardiac function. Furthermore, the amplitude of stress-stimulated mitophagic activity could be modulated by AMPKα2.

This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

99686

AMPK regulates Bcl2-L-13-mediated mitophagy induction for cardioprotection

Elsevier B.V.

英語

2024-12-24

Cell Reports

43

12

115001

https://doi.org/10.1016/j.celrep.2024.115001

https://hdl.handle.net/11094/99686