Open AccessJournal Article
Cyclosporin-induced endothelial cell injury
349
TL;DR: It is indicated that CyA exerts a direct cytotoxic effect on endothelial cells and might help in understanding the pathogenesis of CyA-induced vascular damage.
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About: This article is published in Laboratory Investigation. The article was published on 01 Oct 1986. and is currently open access. The article focuses on the topics: Endothelial stem cell & Endothelium.
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Citations
Immunosuppressive treatment of aortic allografts
TL;DR: It is concluded that a low maintenance dose of CsA provides effective immunosuppression, thereby preventing aneurysm formation, and that the potential use of arterial allografts in vascular surgery may need to be readdressed.
137
Detection of microhemorrhage in posterior reversible encephalopathy syndrome using susceptibility-weighted imaging
TL;DR: SWI showed a higher rate of MH than previously described, underscoring the potential of SWI in evaluating PRES and proposing that MHs in PRES relate to endothelial cell dysfunction.
129
Arginine feeding modifies cyclosporine nephrotoxicity in rats.
TL;DR: It is suggested that chronic CsA may diminish NO activity within the kidney, and that this capacity may be partially restored by arginine feeding.
Post-cyclosporine-mediated hypertension and nephropathy: amelioration by vascular endothelial growth factor.
Duk Hee Kang,Yoon Goo Kim,Yoon Goo Kim,Takeshi F. Andoh,Katherine L. Gordon,Shinichi Suga,Marilda Mazzali,J. Ashley Jefferson,Jeremy Hughes,William M. Bennett,George F. Schreiner,Richard J. Johnson +11 more
TL;DR: CsA-associated renal microvascular and tubulointerstitial injury results in the development of salt-sensitive hypertension and treatment of animals with established CsA nephropathy with VEGF reduces the hypertensive response and accelerates histological recovery, which may be due to the improvement of arteriolopathy.
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Inhibition ofAtherosclerosis inCD4T-Cell-Ablated andNude(nu/fu) C57BL/6 Hyperlipidemic Mice
Mei-Ling Shen
- 01 Jan 1996
TL;DR: It is suggested that in these two models T lymphocytes contribute to the pathogenesis of early atherosclerotic lesions and that a further understanding of this phenomenon may provide future approaches toward the prevention and treatment of the disease.
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