ArticleCell death & disease2023
DAPL1 prevents epithelial-mesenchymal transition in the retinal pigment epithelium and experimental proliferative vitreoretinopathy.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- Olink proteomics profiling platform reveals inflammatory protein biomarkers in vitreous with different degrees of proliferative vitreoretinopathy.Eye (London, England) · 2026Article
- DAPL1 restrains RPE PANoptosis in experimental AMD by inhibiting GRP75-mediated mitochondria-associated endoplasmic reticulum membranes.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- DAPL1 is activated by Np63 and GRα and regulates lipid metabolism.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Vaccinia-related kinase 1/snail family transcriptional repressor 1 regulates epithelial-mesenchymal transition and inflammation in proliferative vitreoretinopathy.International journal of ophthalmology · 2026Article
- JNK inhibitor SP600125 alleviates TGF-β2-induced epithelial-mesenchymal transition in RPE cellInternational journal of ophthalmology · 2026Article
- Cannabidiol inhibits TGF-β1-induced epithelial-mesenchymal transition in human conjunctival epithelial cells by interrupting TGF-β/Smad signaling.Scientific reports · 2025Article
- DAPL1 inhibits epithelial-mesenchymal transition of retinal pigment epithelial cells by regulating the TGF-β/MITF pathway.Experimental eye research · 2025Article
- A Dapl1Science advances · 2025Article
- Leveraging AAV1-Rac1T17N to prevent experimental proliferative vitreoretinopathy.Journal of translational medicine · 2025Article
- Klotho attenuates epithelial‑mesenchymal transition of retinal pigment epithelial cells in subretinal fibrosis by suppressing the ERK1/2 and Wnt/β‑catenin signaling pathways.International journal of molecular medicine · 2025Article
- Death associated protein like 1 acts as a novel tumor suppressor in melanoma by increasing the stability of P21 protein.Molecular and cellular biochemistry · 2025Article
- Absent in melanoma 2: a potent suppressor of retinal pigment epithelial-mesenchymal transition and experimental proliferative vitreoretinopathy.Cell death & disease · 2025Article
- Article
- The retinal pigment epithelium: Functions and roles in ocular diseases.Fundamental research · 2024Review
- ABCA4 mediated traumatic proliferative vitreoretinopathy associated with PI3K/Akt signaling pathway.Heliyon · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) of the retinal pigment epithelium (RPE) is a hallmark of the pathogenesis of proliferative vitreoretinopathy (PVR) that can lead to severe vision loss. Nevertheless, the precise regulatory mechanisms underlying the pathogenesis of PVR remain largely unknown. Here, we show that the expression of death-associated protein-like 1 (DAPL1) is downregulated in PVR membranes and that DAPL1 deficiency promotes EMT in RPE cells in mice. In fact, adeno-associated virus (AAV)-mediated DAPL1 overexpression in RPE cells of Dapl1-deficient mice inhibited EMT in physiological and retinal-detachment states. In a rabbit model of PVR, ARPE-19 cells overexpressing DAPL1 showed reduced ability to induce experimental PVR, and AAV-mediated DAPL1 delivery attenuated the severity of experimental PVR. Furthermore, a mechanistic study revealed that DAPL1 promotes P21 phosphorylation and its stabilization partially through NFκB (RelA) in RPE cells, whereas the knockdown of P21 led to neutralizing effects on DAPL1-dependent EMT inhibition and enhanced the severity of experimental PVR. These results suggest that DAPL1 acts as a novel suppressor of RPE-EMT and has an important role in antagonizing the pathogenesis of experimental PVR. Hence, this finding has implications for understanding the mechanism of and potential therapeutic applications for PVR.
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