Commentary 10.1172/JCI129704
1Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, USA.
2G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, Mississippi, USA.
Address correspondence to: Michael J. Ryan, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, Mississippi 39216-4505. Email: mjryan@umc.edu.
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1Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi, USA.
2G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, Mississippi, USA.
Address correspondence to: Michael J. Ryan, Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, Mississippi 39216-4505. Email: mjryan@umc.edu.
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Ryan, M.
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First published June 17, 2019 - More info
Multiple myeloma (MM) is a relatively common hematologic malignancy, and up to half of patients with MM present with renal dysfunction at the time of diagnosis. MM-associated renal injury has been linked to an excess level of monoclonal immunoglobulin free light chains (FLCs) in the circulation; however, it is not clear how these FLCs drive renal pathology. In this issue of the JCI, Ying et al. unravel a novel mechanism by which FLCs mediate renal injury in MM by inducing fibrotic and inflammatory pathways in the kidney. Specifically, FLC-mediated production of H2O2 was shown to activate JAK2/STAT1 signaling, increase production of IL-1β via induction of capsase-1, and promote activation of TGF-β via αvβ6 integrin. Moreover, the authors identified a tryptophan residue within a specific monoclonal FLC that was required for optimal H2O2 production and downstream signaling. A better understanding of the drivers of MM-associated renal injury has potential for the identification of promising therapeutic targets.
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