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Review
. 2023 Jan 22;15(3):680.
doi: 10.3390/cancers15030680.

Endothelial Dysfunction Syndromes after Allogeneic Stem Cell Transplantation

Affiliations
Review

Endothelial Dysfunction Syndromes after Allogeneic Stem Cell Transplantation

Dionysios Vythoulkas et al. Cancers (Basel). .

Abstract

Allogeneic hematopoietic stem cell transplantation (allo-HSCT) remains the only therapy with a curative potential for a variety of malignant and non-malignant diseases. The major limitation of the procedure is the significant morbidity and mortality mainly associated with the development of graft versus host disease (GVHD) as well as with a series of complications related to endothelial injury, such as sinusoidal obstruction syndrome/veno-occlusive disease (SOS/VOD), transplant-associated thrombotic microangiopathy (TA-TMA), etc. Endothelial cells (ECs) are key players in the maintenance of vascular homeostasis and during allo-HSCT are confronted by multiple challenges, such as the toxicity from conditioning, the administration of calcineurin inhibitors, the immunosuppression associated infections, and the donor alloreactivity against host tissues. The early diagnosis of endothelial dysfunction syndromes is of paramount importance for the development of effective prophylactic and therapeutic strategies. There is an urgent need for the better understanding of the pathogenetic mechanisms as well as for the identification of novel biomarkers for the early diagnosis of endothelial damage. This review summarizes the current knowledge on the biology of the endothelial dysfunction syndromes after allo-HSCT, along with the respective therapeutic approaches, and discusses the strengths and weaknesses of possible biomarkers of endothelial damage and dysfunction.

Keywords: allogeneic stem cell transplantation; biomarkers; dysfunction; endothelial cell; graft-versus-host disease.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Idipathic Pneumonia Syndrome.
Figure 2
Figure 2
Pathogenesis of endothelial dysfunction syndromes.

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