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The activation of LBH-CRYAB signaling promotes cardiac protection against I/R injury by inhibiting apoptosis and ferroptosis.
- Source :
-
IScience [iScience] 2024 Mar 15; Vol. 27 (5), pp. 109510. Date of Electronic Publication: 2024 Mar 15 (Print Publication: 2024). - Publication Year :
- 2024
-
Abstract
- Myocardial ischemia-reperfusion (I/R) injury stands out among cardiovascular diseases, and current treatments are considered unsatisfactory. For cardiomyocytes (CMs) in ischemic tissues, the upregulation of Limb-bud and Heart (LBH) and αB-crystallin (CRYAB) and their subsequent downregulation in the context of cardiac fibrosis have been verified in our previous research. Here, we focused on the effects and mechanisms of activated LBH-CRYAB signaling on damaged CMs during I/R injury, and confirmed the occurrence of mitochondrial apoptosis and ferroptosis during I/R injury. The application of inhibitors, ectopic expression vectors, and knockout mouse models uniformly verified the role of LBH in alleviating both apoptosis and ferroptosis of CMs. p53 was identified as a mutual downstream effector for both LBH-CRYAB-modulated apoptosis and ferroptosis inhibition. In mouse models, LBH overexpression was confirmed to exert enhanced cardiac protection against I/R-induced apoptosis and ferroptosis, suggesting that LBH could serve as a promising target for the development of I/R therapy.<br />Competing Interests: The authors have declared that no competing interests exists.<br /> (© 2024 The Authors. Published by Elsevier Inc.)
Details
- Language :
- English
- ISSN :
- 2589-0042
- Volume :
- 27
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- IScience
- Publication Type :
- Academic Journal
- Accession number :
- 38660406
- Full Text :
- https://doi.org/10.1016/j.isci.2024.109510