ArticleiScience2024
The activation of LBH-CRYAB signaling promotes cardiac protection against I/R injury by inhibiting apoptosis and ferroptosis.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
- Usnic acid inhibits colorectal cancer liver metastasis by targeting CRYAB phosphorylation and inducing ferroptosis.Cell communication and signaling : CCS · 2026Article
- αB-Crystallin Protects Against Cisplatin-Induced Nephrotoxicity by Modulating Apoptosis In Vivo and In Vitro.Current issues in molecular biology · 2026Article
- Reliable Identification of Cardiac Maturation Markers Using Robust and Flexible Label-Free Proteomic Quantitation by Spectral Counting on Relatively Abundant Proteins.Journal of proteome research · 2026Article
- Targeting the ARRDC3-DRP1 Axis via hUMSC-Derived Exosomal CRYAB for Neuroprotection in Cerebral Ischemia/Reperfusion Injury.Advanced healthcare materials · 2026Article
- Crosstalk between autophagy-dependent ferroptosis and PANoptosis in myocardial and cerebral ischemia-reperfusion injury: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Quercetin attenuates ferroptosis-associated myocardial injury in rats after coronary microembolization by activating the Nrf2/HO-1 signaling pathway.Iranian journal of basic medical sciences · 2026Article
- PTMA controls cardiomyocyte proliferation and cardiac repair by enhancing STAT3 acetylation.Science advances · 2025Article
- Article
- Ferroptosis-Related Gene CRYAB in Asthma: Bioinformatics Identification and Experimental Validation.Journal of inflammation research · 2025Article
- Whole Exome Sequencing Reveals Novel Genetic Variants Associated with Atrial Septal Defect in a Tibetan Patient Cohort.Pharmacogenomics and personalized medicine · 2025Article
- Cardamonin Attenuates Myocardial Ischemia/Reperfusion-Induced Ferroptosis Through Promoting STAT3 Signaling.Journal of inflammation research · 2024Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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