Transplant-associated thrombotic microangiopathy (TA-TMA) is a severe complication in patients after hematopoietic stem cell transplantation. The pathogenesis of TA-TMA is still unclear. Previous studies showed that complement activation plays an important role in the development of TA-TMA. However, no data showed which kind of complement component triggers this process.

Recently, Prof. Han‘s group from Jiangsu Institute of Hematology developed a heme oxygenase-1, which could induce decay-accelerating factor (DAF) and inhibit the membrane-attack complex, was significantly decreased in patients with TA-TMA. DAF levels in the TA-TMA group were in line with the levels in the myocardial infarction group but were lower than levels in the healthy, non-complication, infection, and graft-versus-host disease groups (P < 0.05). Human umbilical vein endothelial cells (HUVECs) incubated with TA-TMA plasma showed lower DAF levels compared with that incubated with normal human plasma. Notably, treatment with N-acetylcysteine (NAC), a drug against oxidation, increased the level of DAF. NAC could also inhibit complement activation in HUVECs incubated with TA-TMA plasma. Taken together, we propose that NAC represent a new potential therapy for patients facing TA-TMA. Their work has been published in Biol Blood Marrow Transplant (Biol Blood Marrow Transplant. 2019 ;25(8):1486-1491), titled as “Circulating Heme Oxygenase-1 and Complement Activation in Transplant-Associated Thrombotic Microangiopathy”.

Link to Paper：https://www.sciencedirect.com/science/article/pii/

Link to Prof. Han’ group：http://fyy.sdfyy.cn/Article/detail/id/59482.html