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Figure 4

Descripción

In vitro endothelial-to-mesenchymal transition markers are quantified following NET exposure, demonstrating increased mesenchymal and decreased endothelial protein expression.

More Figures from This Paper

The molecular mechanism linking NET-derived DNA to Hippo-YAP pathway inhibition and endothelial-to-mesenchymal transition is elucidated, with DNase treatment as a potential therapeutic approach.

Figure 3

The molecular mechanism linking NET-derived DNA to Hippo-YAP pathway inhibition and endothelial-to-mesenchymal transition is elucidated, with DNase treatment as a potential therapeutic approach.

diagram
YAP phosphorylation and nuclear exclusion in NET-treated endothelial cells are characterized, linking NET exposure to Hippo pathway activation.

Figure 5

YAP phosphorylation and nuclear exclusion in NET-treated endothelial cells are characterized, linking NET exposure to Hippo pathway activation.

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Wound healing outcomes in Padi4-knockout diabetic mice compared to wild-type controls are documented, showing accelerated closure when NET formation is genetically ablated.

Figure 6

Wound healing outcomes in Padi4-knockout diabetic mice compared to wild-type controls are documented, showing accelerated closure when NET formation is genetically ablated.

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Histological analysis of wound tissue from NET-depleted and control diabetic mice reveals improved re-epithelialization and vascularization.

Figure 7

Histological analysis of wound tissue from NET-depleted and control diabetic mice reveals improved re-epithelialization and vascularization.

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DNase I treatment effects on diabetic wound healing in vivo are quantified, demonstrating that NET degradation promotes wound closure through preserved endothelial function.

Figure 8

DNase I treatment effects on diabetic wound healing in vivo are quantified, demonstrating that NET degradation promotes wound closure through preserved endothelial function.

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A proposed model integrating NET-mediated Hippo pathway suppression with endothelial-to-mesenchymal transition in delayed diabetic wound healing is diagrammed.

Figure 9

A proposed model integrating NET-mediated Hippo pathway suppression with endothelial-to-mesenchymal transition in delayed diabetic wound healing is diagrammed.

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Figure 4

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Source Paper

Neutrophil Extracellular Traps Delay Diabetic Wound Healing by Inducing Endothelial-to-Mesenchymal Transition via the Hippo pathway.

International journal of biological sciences (2023)

PMID: 36594092

DOI: 10.7150/ijbs.78046

Cite This Figure

![Figure 4: In vitro endothelial-to-mesenchymal transition markers are quantified following NET exposure, demonstrating increased mesenchymal and decreased endothelial protein expression.](https://pdfs.citedhealth.com/figures/36594092/193.png)

> Source: Shuofei Yang et al. "Neutrophil Extracellular Traps Delay Diabetic Wound Healing by Inducing Endothel." *International journal of biological sciences*, 2023. PMID: [36594092](https://pubmed.ncbi.nlm.nih.gov/36594092/)
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  <img src="https://pdfs.citedhealth.com/figures/36594092/193.png" alt="In vitro endothelial-to-mesenchymal transition markers are quantified following NET exposure, demonstrating increased mesenchymal and decreased endothelial protein expression." />
  <figcaption>Figure 4. In vitro endothelial-to-mesenchymal transition markers are quantified following NET exposure, demonstrating increased mesenchymal and decreased endothelial protein expression.<br>  Source: Shuofei Yang et al. "Neutrophil Extracellular Traps Delay Diabetic Wound Healing by Inducing Endothel." <em>International journal of biological sciences</em>, 2023. PMID: <a href="https://pubmed.ncbi.nlm.nih.gov/36594092/">36594092</a></figcaption>
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