Successful Treatment of Mitochondrial Toxicity in an HIV-Positive Patient After Liver Transplantation

Kim, I.K.; Gaultier, Cyril R.; Steggerda, Justin; Pan, Shenyi; Klein, Andrew S.; Annamalai, A.; Tran, Tai Ngoc; Nissen, N.

doi:10.1016/j.transproceed.2015.10.010

Cited by 2 publications

(1 citation statement)

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“…Liver graft fibrosis in particular is a major determinant of clinical outcomes in CLAD patients [5]. These histopathologic changes associated with CLAD can be attributed to immunological and nonimmunological factors, including ischemia/reperfusion (I/R) injury, acute or chronic rejection, drug toxicity, and de novo or recurrent disease [6, 7]. Development of novel strategies that prevent CLAD-associated damage is the key to ultimate graft survival.…”

Section: Introductionmentioning

confidence: 99%

CXCL4 Contributes to the Pathogenesis of Chronic Liver Allograft Dysfunction

Liu

Shi

et al. 2016

Journal of Immunology Research

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Chronic liver allograft dysfunction (CLAD) remains the most common cause of patient morbidity and allograft loss in liver transplant patients. However, the pathogenesis of CLAD has not been completely elucidated. By establishing rat CLAD models, in this study, we identified the informative CLAD-associated genes using isobaric tags for relative and absolute quantification (iTRAQ) proteomics analysis and validated these results in recipient rat liver allografts. CXCL4, CXCR3, EGFR, JAK2, STAT3, and Collagen IV were associated with CLAD pathogenesis. We validated that CXCL4 is upstream of these informative genes in the isolated hepatic stellate cells (HSC). Blocking CXCL4 protects against CLAD by reducing liver fibrosis. Therefore, our results indicated that therapeutic approaches that neutralize CXCL4, a newly identified target of fibrosis, may represent a novel strategy for preventing and treating CLAD after liver transplantation.

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Section: Introductionmentioning

confidence: 99%