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논문분류	춘계학술대회 초록집
제목	New Target Alleviates Acute Kidney Injury by Modulating Inflammatory Signaling and Immune Remodeling
저자	Jeongseon Oh
출판정보	2026; 2026(1):
키워드	Acute kidney injury, Ischemia-reperfusion injury, Inflammation
초록	Objectives: Renal ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI), characterized by tubular epithelial damage and robust inflammatory activation involving leukocyte recruitment. In this study, we identify membrane protein K as a previously unrecognized regulator that integrates inflammatory signaling with renal immune remodeling and tubular stress responses during IRI-induced AKI. Methods: Renal ischemia–reperfusion injury (IRI) was induced in wild-type and membrane protein K–knockout mice, by bilateral renal pedicle clamping, with analysis performed 24 hours after reperfusion. Recombinant membrane protein K was administered in selected groups. Renal function, histology, cytokine profiles, and intrarenal leukocyte populations were assessed using biochemical assays, histopathology, multiplex cytokine analysis, and flow cytometry. HK-2 cells were exposed to CoCl₂ to model hypoxic stress, and proliferation, inflammatory gene expression, and apoptosis-related signaling were evaluated. Results: At 24 hours after renal IRI, genetic deletion of membrane protein K resulted in aggravated renal injury, accompanied by altered systemic cytokine profiles and remodeling of intrarenal leukocyte populations, including significant changes within the renal CD45⁺ compartment. Conversely, supplementation with recombinant membrane protein K protein attenuated renal injury, restored inflammatory balance, and normalized intrarenal immune composition. To further investigate tubular epithelial responses under hypoxia-like stress, HK-2 cells were exposed to CoCl₂ to model injury. Membrane protein K modulated epithelial cell proliferation and inflammatory gene expression and was associated with anti-apoptotic signaling in hypoxia mimic conditions. Conclusion: Collectively, these findings establish membrane protein K as a dual immune and epithelium modulatory mediator that coordinates inflammatory signaling, leukocyte remodeling, and tubular stress resilience in IRI-driven AKI, supporting its potential as a therapeutic target for early kidney injury.
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