ArticleNature communications2024
Dysregulated RBM24 phosphorylation impairs APOE translation underlying psychological stress-induced cardiovascular disease.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- RNA-binding proteins in aging and age-related diseases: roles, mechanisms, and a large language model analysis.Biogerontology · 2026Review
- Temporal trends in myocardial ischemia risk estimated from 12-lead electrocardiograms using deep learning in individuals with suspected cancer during health checkups.Cardio-oncology (London, England) · 2026Article
- Different mRNAs encoding identical proteins: how and why?Journal of applied genetics · 2026Article
- Integrated transcriptomic and proteomic analysis reveals inhibitory effects of naringenin application on soybean roots mainly by interfering with auxin and ROS concentrations.BMC plant biology · 2026Article
- Multi-omics and comprehensive multi-trait analysis identify shared genetic etiology of heart failure and related cancers.Human genomics · 2025Article
- TRIM21-driven K63-linked ubiquitination of RBM38c, as a novel interactor of BECN1, contributes to DNA damage-induced autophagy.Cell death and differentiation · 2025Article
- Chronic Psychological Stress in Oncogenesis: Multisystem Crosstalk and Multimodal Interventions.Research (Washington, D.C.) · 2025Review
- Evolutionary Conservation and Functional Diversification of the Rbm24/38 Family in Metazoans.Wiley interdisciplinary reviews. RNAReview
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Authors and funding
22 authors.
Funding
Abstract
Psychological stress contributes to cardiovascular disease (CVD) and sudden cardiac death, yet its molecular basis remains obscure. RNA binding protein RBM24 plays a critical role in cardiac development, rhythm regulation, and cellular stress. Here, we show that psychological stress activates RBM24 S181 phosphorylation through eIF4E2-GSK3β signaling, which causally links psychological stress to CVD by promoting APOE translation (apolipoprotein E). Using an Rbm24 S181A KI mouse model, we show that impaired S181 phosphorylation leads to cardiac contractile dysfunction, atrial fibrillation, dyslipidemia, reduced muscle strength, behavioral abnormalities, and sudden death under acute and chronic psychological stressors. The impaired S181 phosphorylation of RBM24 inhibits cardiac translation, including APOE translation. Notably, cardiomyocyte-specific expression of APOE rescues cardiac electrophysiological abnormalities and contractile dysfunction, through preventing ROS stress and mitochondrial dysfunction. Moreover, RBM24-S181 phosphorylation acts as a serum marker for chronic stress in human. These results provide a functional link between RBM24 phosphorylation, eIF4E-regulated APOE translation, and psychological-stress-induced CVD.
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Registered trials
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