# Endothelial-Related Gene Expression Plays a Role Against Acute Kidney Injury and Prolonged Intensive Care Stay in Liver Allografts Treated with Hypothermic Oxygenated Perfusion

**Authors:** Francesco Vasuri, Carmen Ciavarella, Giuliana Germinario, Deborah Malvi, Luca Saragoni, Antonia D’Errico, Matteo Ravaioli, Gianandrea Pasquinelli

PMC · DOI: 10.3390/medsci14010087 · Medical Sciences · 2026-02-12

## TL;DR

This study shows that gene activity related to blood vessels can predict recovery and complications after liver transplants using a new preservation method.

## Contribution

The study identifies endothelial-related gene expression as a novel predictor of post-transplant outcomes and acute kidney injury.

## Key findings

- Higher expression of SMA, ERG, and TGF-β1 correlates with shorter ICU stays after liver transplantation.
- SMA and TGF-β1 expression is significantly linked to arteriolar myointimal thickening in liver grafts.
- Endothelial gene activity is associated with reduced acute kidney injury risk post-transplant.

## Abstract

Background: Hypothermic oxygenated perfusion (HOPE) has emerged as a promising preservation strategy before liver transplantation, mitigating ischemia–reperfusion injury and improving graft function, especially in marginal grafts and donors after cardiac death. Methods: This is a prospective monocentric study; 34 HOPE-treated liver grafts were enrolled and analyzed through histopathology and RT-PCR to assess endothelial-related gene expression and its correlation with post-transplant outcome. The aim of the present study was to assess the relationship between the expression of genes related to vascular activation and homeostasis and post-transplant clinical characteristics. Results: Expression of SMA and TGF-β1 was significantly associated with arteriolar myointimal thickening of the graft (p = 0.007 and 0.068). Higher expression of SMA, ERG, and TGF-β1 was correlated with a shorter post-operative intensive care stay (p = 0.070, p = 0.010 and p = 0.029, respectively), particularly with post-transplant acute kidney injury. Conclusions: These findings highlight the role of endothelial activation and vascular homeostasis for an early recovery after liver transplantation, posing an important issue for healthcare systems as well, and suggesting molecular markers for graft assessment and risk stratification.

## Linked entities

- **Genes:** SMN1 (survival of motor neuron 1, telomeric) [NCBI Gene 6606], TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040], ERG (ETS transcription factor ERG) [NCBI Gene 2078]
- **Diseases:** acute kidney injury (MONDO:0002492)

## Full-text entities

- **Genes:** TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, KDR (kinase insert domain receptor) [NCBI Gene 3791] {aka CD309, FLK1, VEGFR, VEGFR2}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, SMN1 (survival of motor neuron 1, telomeric) [NCBI Gene 6606] {aka BCD541, GEMIN1, SMA, SMA1, SMA2, SMA3}, CD34 (CD34 molecule) [NCBI Gene 947], ERG (ETS transcription factor ERG) [NCBI Gene 2078] {aka LMPHM14, erg-3, p55}, GAPDH (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 2597] {aka G3PD, GAPD, HEL-S-162eP}, ACTA1 (actin alpha 1, skeletal muscle) [NCBI Gene 58] {aka ACTA, ASMA, CFTD, CFTD1, CFTDM, CMYO2A}
- **Diseases:** post (MESH:D000094025), end-stage liver failure (MESH:D007676), cholestasis (MESH:D002779), graft failure (MESH:D051437), Lobular necrosis (MESH:D018275), POIC (MESH:C000657744), EAD (MESH:D055031), vascular damage (MESH:D057772), reperfusion injury (MESH:D015427), MELD (MESH:D058625), fibrosis (MESH:D005355), Portal inflammation (MESH:D007249), injury to (MESH:D014947), portal fibrosis (MESH:D000094724), DCD (MESH:D003643), head trauma (MESH:D006259), necrosis (MESH:D009336), liver cancers (MESH:D006528), ischemia (MESH:D007511), Bile duct regression (MESH:D001649), HOPE (MESH:D000860), allograft dysfunction (MESH:D000092122), anoxic encephalopathy (MESH:D002534), DBD (MESH:D001926), extrahepatic organ dysfunction (MESH:D009102), biliary damage (MESH:D001660), brain hemorrhage (MESH:D020300), macrovesicular steatosis (MESH:D005234), LT (MESH:D017093), stroke (MESH:D020521), AKI (MESH:D058186), hepatitis (MESH:D056486)
- **Chemicals:** Bilirubin (MESH:D001663), paraffin (MESH:D010232), HOPE (-), nitric oxide (MESH:D009569), formalin (MESH:D005557), SYBR green (MESH:C098022)
- **Species:** Homo sapiens (human, species) [taxon 9606], Rodentia (rodent, order) [taxon 9989]

## Full text

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## Figures

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## References

24 references — full list in the complete paper: https://tomesphere.com/paper/PMC12921878/full.md

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Source: https://tomesphere.com/paper/PMC12921878