ArticleSignal transduction and targeted therapy2025
Nucleosome assembly protein-like 1 degradation-dependent novel cardioprotection mechanism of Wnt2 against ischemia‒reperfusion injury.
Article in Signal transduction and targeted therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Ubiquitination-dependent regulation of ferroptosis in ischemic heart and brain.Redox biology · 2026Review
- CPTCs Drive Somatic-Visceral Communication via the Wnt Axis in Somatic Mechanotherapy: A Single-Cell Deep Learning Study.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Landscape of Immune Remodeling and NAP1L1-Driven Epithelial Reprogramming in Gastric Cancer Metastasis.Chronic diseases and translational medicine · 2026Article
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14 authors.
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Abstract
Wnt and its crosstalk signaling pathways are involved in the modulating ischemia‒reperfusion (I/R) injury. However, whether Wnt2 is a novel therapeutic agent for I/R injury is largely unknown. Here, we show that the downregulation of serum Wnt2 levels in acute myocardial infarction (AMI) patients following reperfusion therapy, and Wnt2 levels are inversely correlated with the levels of myocardial injury markers (cTnT and CK-MB). Therapeutic administration of recombinant Wnt2 protein (rbWnt2) alleviates cardiac I/R injury and improves cardiac function by suppressing ROS levels and cardiomyocyte death in mice. Further analysis revealed that rbWnt2 downregulated Nap1L1 to reactivate the transcription of antioxidant genes (SOD, GPX, and UCP3) to reduce ROS levels and subsequently inhibit cardiomyocyte apoptosis and ferroptosis during the I/R process. Cardiac-specific Nap1L1 knockdown attenuated I/R injury, whereas overexpression of Nap1L1 partly abolished the cardiac protection mediated by rbWnt2 administration in the I/R model. Mechanistically, Wnt2 promoted Nap1L1 ubiquitination and degradation to restore ROS scavenging systems via Lrp6-mediated recruitment of the E3 ligase Trim11 in I/R hearts. Nap1L1 suppression plays a critical role in mediating the cardioprotective effects of rbWnt2. These findings establish Wnt2 as a therapeutic agent that targets compartmentalized oxidative damage, suggesting a novel strategy to mitigate I/R injury through the Lrp6/Trim11/Nap1L1 axis.
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