SLC39A8-mediated zinc dyshomeostasis potentiates kidney disease

Z Zhaoxian Cai (The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine) X Xiaotian Wu (The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine) T Tianyi Wang (Advanced Institute for Materials Research (WPI-AIMR)) Z Zijun Song (The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine) P Pu Ni (The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine) M Meijuan Zhong (School of Public Health, Basic Medical Sciences, The First Affiliated Hospital, Hengyang Medical School, University of South China) Y Yunxing Su (The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine) E Enjun Xie (The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine) S Shumin Sun (Institute of Functional Nano & Soft Materials (FUNSOM), Jiangsu Key Laboratory for Carbon-Based Functional Materials and Devices) Y Yangjun Lin (The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine) J Junxia Min (The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine) F Fudi Wang (The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine)

Abstract

While numerous genetic risk loci are linked to kidney disease, a unifying therapeutic target for diverse renal pathologies remains elusive. Here, through large-cohort polymorphic locus screening, we identify the SLC39A8 A391T variant (rs13107325) as a shared modifier of multiple kidney diseases. Functional characterization using Slc39a8 A391T knock-in mice and kidney-specific Slc39a8 knockout mice reveals that loss of SLC39A8 function reduces renal zinc accumulation, thereby mitigating susceptibility to kidney injury and disease progression. Mechanistically, we demonstrate that perturbed zinc homeostasis drives renal damage, and limiting zinc levels—whether via impaired SLC39A8 activity or direct chelation—activates the zinc–AKT–FOXO1–G6PC axis to confer protection. Critically, zinc chelation with EDTA recapitulates this benefit, significantly preventing and ameliorating experimental acute and chronic kidney disease. These findings establish renal zinc homeostasis as a key therapeutic node, with SLC39A8 and zinc-modulating strategies representing promising avenues for treating a broad range of kidney diseases.

Article Details

Volume / Issue Vol. 122, Issue 38
Published September 23, 2025
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (12)

Z

Zhaoxian Cai

The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine

X

Xiaotian Wu

The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine

T

Tianyi Wang

Advanced Institute for Materials Research (WPI-AIMR)

Z

Zijun Song

The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine

P

Pu Ni

The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine

M

Meijuan Zhong

School of Public Health, Basic Medical Sciences, The First Affiliated Hospital, Hengyang Medical School, University of South China

Y

Yunxing Su

The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine

E

Enjun Xie

The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine

S

Shumin Sun

Institute of Functional Nano & Soft Materials (FUNSOM), Jiangsu Key Laboratory for Carbon-Based Functional Materials and Devices

Y

Yangjun Lin

The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine

J

Junxia Min

The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine

F

Fudi Wang

The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine