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dc.contributor.authorMaarouf, O.H.
dc.contributor.authorUehara, M.
dc.contributor.authorKasinath, V.
dc.date.accessioned2019-06-21T18:46:26Z
dc.date.available2019-06-21T18:46:26Z
dc.date.issued2018
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85052559435&doi=10.1172%2fjci.insight.120546&partnerID=40&md5=93aa524f3d4ba87073a7119779905a37
dc.identifier.urihttp://hdl.handle.net/10713/9685
dc.description.abstractThe contribution of the kidney-draining lymph node (KLN) to the pathogenesis of ischemia-reperfusion injury (IRI) of the kidney and its subsequent recovery has not been explored in depth. In addition, the mechanism by which repetitive IRI contributes to renal fibrosis remains poorly understood. Herein, we have found that IRI of the kidney is associated with expansion of high endothelial venules (HEVs) and activation of fibroblastic reticular cells (FRCs) in the KLN, as demonstrated by significant expansion in the extracellular matrix. The lymphotoxin α signaling pathway mediates activation of FRCs, and chronic treatment with lymphotoxin β receptor-immunoglobulin fusion protein (LTβr-Ig) resulted in marked alteration of the KLN as well as augmentation of renal fibrosis. Depletion of FRCs reduced T cell activation in the KLN and ameliorated renal injury in acute IRI. Repetitive renal IRI was associated with senescence of FRCs, fibrosis of the KLN, and renal scarring, which were ameliorated by FRC administration. Therefore, our study emphasizes the critical role of FRCs in both the initiation and repair phases of injury following IRI of the kidney.en_US
dc.description.urihttps://dx.doi.org/10.1172/jci.insight.120546en_US
dc.language.isoen-USen_US
dc.publisherAmerican Society for Clinical Investigationen_US
dc.relation.ispartofJCI insight
dc.subjectChronic kidney diseaseen_US
dc.subjectFibrosisen_US
dc.subjectNephrologyen_US
dc.titleRepetitive ischemic injuries to the kidneys result in lymph node fibrosis and impaired healingen_US
dc.typeArticleen_US
dc.identifier.doi10.1172/jci.insight.120546
dc.identifier.pmid29997302


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