Recent advances in the role of mammalian target of rapamycin inhibitors on cardiac allograft vasculopathy

2019 ◽  
Vol 34 (1) ◽  
Author(s):  
Lavanya Bellumkonda ◽  
Jignesh Patel
2020 ◽  
Vol 39 (4) ◽  
pp. S76
Author(s):  
M. Pazdernik ◽  
J. Hubacek ◽  
P. Wohlfahrt ◽  
J. Kautzner ◽  
V. Melenovsky ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhenggang Zhang ◽  
Na Zhang ◽  
Junyu Shi ◽  
Chan Dai ◽  
Suo Wu ◽  
...  

The role of IL-33/ST2 signaling in cardiac allograft vasculopathy (CAV) is not fully addressed. Here, we investigated the role of IL-33/ST2 signaling in allograft or recipient in CAV respectively using MHC-mismatch murine chronic cardiac allograft rejection model. We found that recipients ST2 deficiency significantly exacerbated allograft vascular occlusion and fibrosis, accompanied by increased F4/80+ macrophages and CD3+ T cells infiltration in allografts. In contrast, allografts ST2 deficiency resulted in decreased infiltration of F4/80+ macrophages, CD3+ T cells and CD20+ B cells and thus alleviated vascular occlusion and fibrosis of allografts. These findings indicated that allografts or recipients ST2 deficiency oppositely affected cardiac allograft vasculopathy/fibrosis via differentially altering immune cells infiltration, which suggest that interrupting IL-33/ST2 signaling locally or systematically after heart transplantation leads different outcome.


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