Skip to main content
ImmuneCited
Figure 5

Mô tả

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

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

Figure 4

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

chart
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.

chart
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.

micrograph
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.

chart
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.

diagram

Figure 5

Chart
989 × 673px · 306,1 KB

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 5: YAP phosphorylation and nuclear exclusion in NET-treated endothelial cells are characterized, linking NET exposure to Hippo pathway activation.](https://pdfs.citedhealth.com/figures/36594092/203.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/)
<figure>
  <img src="https://pdfs.citedhealth.com/figures/36594092/203.png" alt="YAP phosphorylation and nuclear exclusion in NET-treated endothelial cells are characterized, linking NET exposure to Hippo pathway activation." />
  <figcaption>Figure 5. YAP phosphorylation and nuclear exclusion in NET-treated endothelial cells are characterized, linking NET exposure to Hippo pathway activation.<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>
</figure>

Bằng chứng liên quan

B
Arginine cho Wound Healing and Immune Recovery

Xếp hạng B · 8 nghiên cứu