Corrigendum
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10.1172/jci.insight.198650
Repetitive ischemic injuries to the kidneys result in lymph node fibrosis and impaired healing
Omar H. Maarouf, Mayuko Uehara, Vivek Kasinath, Zhabiz Solhjou, Naima Banouni, Baharak Bahmani, Liwei Jiang, Osman A. Yilmam, Indira Guleria, Scott B. Lovitch, Jane L. Grogan, Paolo Fiorina, Peter T. Sage, Jonathan S. Bromberg, Martina M. McGrath, and Reza Abdi
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Published September 23, 2025 - More info
JCI Insight. 2025;10(20):e198650. https://doi.org/10.1172/jci.insight.198650.
© 2025 Maarouf et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
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Abstract
The 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.
Authors
Omar H. Maarouf, Mayuko Uehara, Vivek Kasinath, Zhabiz Solhjou, Naima Banouni, Baharak Bahmani, Liwei Jiang, Osman A. Yilmam, Indira Guleria, Scott B. Lovitch, Jane L. Grogan, Paolo Fiorina, Peter T. Sage, Jonathan S. Bromberg, Martina M. McGrath, Reza Abdi
Original citation: JCI Insight. 2018;3(13):e120546. https://doi.org/10.1172/jci.insight.120546
Citation for this corrigendum: JCI Insight. 2025;10(20):e198650. https://doi.org/10.1172/jci.insight.198650
The authors recently became aware that that the MECA79-stained KLN:WT panel of Figure 3D is incorrect and was inadvertently uploaded during figure assembly. In addition, the Masson T-stained Kidney: IRI(rep) in supplemental Figure 2A was an inadvertently duplicated from the representative Kidney: LTbr-Ig panel in Figure 4A. The correct figure panels are shown below. The HTML, PDF, and Supplemental Data have been updated online. The authors regret the error.
