# Potential Diagnostic and Therapeutic Uses of DPT in Acute Type A Aortic Dissection

**Authors:** Ting Wei, Xiaopeng Yang, Chao Shi

PMC · DOI: 10.1155/cdr/8896404 · Cardiovascular Therapeutics · 2026-02-06

## TL;DR

This study identifies DPT as a potential diagnostic and therapeutic target for acute Type A aortic dissection, a life-threatening condition with limited treatment options.

## Contribution

The study introduces DPT as a novel biomarker for ATAAD through integrated bioinformatics and experimental validation.

## Key findings

- DPT was found to be downregulated in ATAAD tissues and is associated with aortic wall instability.
- DPT knockdown increased smooth muscle cell migration and reduced proliferation in experimental models.
- DPT showed strong diagnostic potential confirmed by ROC analysis.

## Abstract

Acute Type A aortic dissection (ATAAD) is a catastrophic cardiovascular emergency with high mortality and few treatment options. Diagnostic biomarkers or targeted treatments remain in the rudimentary stage, complicating early detection and intervention. The aim is to discover novel diagnostic and therapeutic biomarkers for ATAAD through integrated bioinformatics and experimental validation.

Differentially expressed genes (DEGs) were identified using the “limma” package in R, applying the combined, normalized, and batch‐effect‐corrected microarray datasets GSE52093 and GSE98770. Functional enrichment analyses (GO and KEGG), protein–protein interaction (PPI) network construction, and weighted gene coexpression network analysis (WGCNA) were performed to identify key genes. Key genes were validated by qPCR, immunofluorescence, and functional assays in human aortic smooth muscle cells (HASMCs) and an independent dataset (GSE153434).

There were 441 DEGs with 164 upregulated and 277 downregulated genes. These hub genes also overlapped with four key genes (DPT, ITGA5, HGF, and PLAUR) in the key WGCNA module. Of these, DPT was downregulated compared with ATAAD tissues. DPT knockdown induced HASMC migration and inhibited HASMC proliferation, as assessed by functional assays. The diagnostic potential of these genes, especially of DPT, was confirmed using ROC analysis.

DPT is a promising diagnostic and therapeutic biomarker for ATAAD. Downregulation may also disturb extracellular matrix homeostasis and smooth muscle cell function, leading to aortic wall instability. These findings provide a foundation for future research on DPT‐targeted interventions for ATAAD.

## Linked entities

- **Genes:** DPT (dermatopontin) [NCBI Gene 1805], ITGA5 (integrin subunit alpha 5) [NCBI Gene 3678], HGF (hepatocyte growth factor) [NCBI Gene 3082], PLAUR (plasminogen activator, urokinase receptor) [NCBI Gene 5329]

## Full-text entities

- **Genes:** HGF (hepatocyte growth factor) [NCBI Gene 3082] {aka DFNB39, F-TCF, HGFB, HPTA, SF}, DPT (dermatopontin) [NCBI Gene 1805] {aka TRAMP}, PLAUR (plasminogen activator, urokinase receptor) [NCBI Gene 5329] {aka CD87, U-PAR, UPAR, URKR}, ITGA5 (integrin subunit alpha 5) [NCBI Gene 3678] {aka CD49e, FNRA, VLA-5, VLA5A}
- **Diseases:** Type A Aortic Dissection (MESH:D000784), ATAAD (MESH:D000094683)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

39 references — full list in the complete paper: https://tomesphere.com/paper/PMC12880953/full.md

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Source: https://tomesphere.com/paper/PMC12880953