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Hematopoietic JAK 2V617F in aortic aneurysms
comparison. Further studies are, thus, needed to validate our findings in larger cohorts.
In conclusion, AA are a possible vascular complication of MPN and hematopoietic JAK2 V617F may causally be involved in the development of AA through macrophage accumulation and MMP activation. The present study also provides novel mechanisms underlying the patho- genesis of AA. Hematopoietic JAK-STAT signaling may be a potential therapeutic target for the development of AA.
Contributions
TY and TM designed the research, performed experiments, analyzed the results, and wrote the manuscript; YK, KW, and KM performed the experiments and analyzed the results; KS and TI interpreted the results and supervised the study; SM and NK analyzed the results and interpreted the results, and super- vised the study; KI designed and supervised the research, ana- lyzed the data, and wrote the manuscript; YT designed and supervised the research, and approved the final version of the manuscript.
Disclosures
TY and KS have received financial support from Janssen Pharmaceutical K.K., Japan; TM has received financial support from Fukuda Denshi Co., Ltd., Japan; Ruxolitinib was provided by Novartis Pharmaceuticals to KI; these companies are, how- ever, not associated with the contents of this study; all other authors declare no conflicts of interest.
Acknowledgments
The authors thank Ms Tomiko Miura and Ms Shoko Sato, from the Department of Cardiovascular Medicine, Fukushima Medical University, Japan, and Ms Chisato Kubo, from the Office for Gender Equality Support, Fukushima Medical University, Japan, for their technical assistance, as well as Prof. Kazuya Shimoda and Dr. Kotaro Shide, from the Department of Gastroenterology and Hematology, University of Miyazaki, Japan, for providing us with JAK2V617F mice.
Funding
This work was supported by JSPS KAKENHI (grant number: JP19K17532) to TY.
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