Erk5-mediated microglial ferroptosis drives ischemic white matter damage via the Nfatc4–Clptm1l axis

Y Yun-Hui Chu (Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology) L Lu-Yang Zhang (Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology) J Jia-Yi He (Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology) Y Ya-Fang Wang (Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology) M Ming-Hao Dong (Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology) Y Yun-Fan You (Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology) X Xiao-Wei Pang (Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology) L Li-Fang Zhu (Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology) H Hang Zhang L Lu-Lu Xu (Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology) L Lian Chen L Luo-Qi Zhou (Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology) J Jun Xiao K Ke Shang (Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology) J Jian-Ke Gong (College of Life Science and Technology, Key Laboratory of Molecular Biophysics of Ministry of Education, Huazhong University of Science and Technology) W Wei Wang D Dai-Shi Tian (Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology) C Chuan Qin (Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology)

Abstract

Ischemic white matter damage is a significant pathological feature of chronic cerebral hypoperfusion, leading to cognitive impairments. However, the underlying molecular mechanisms remain poorly understood. In this study, we identify a causal association between genetically predicted extracellular signal-regulated kinase 5 (ERK5) expression and higher white matter hyperintensity volume through druggable target screening, suggesting its potential as a therapeutic target for white matter damage. Using different animal models of white matter damage, we show that Erk5 expression is significantly upregulated in microglia following both ischemic and demyelinating injury, correlating with the severity of white matter damage. Mechanistically, Erk5 exacerbates white matter damage by promoting microglial ferroptosis through the phosphorylation of nuclear factor of activated T-cells, cytoplasmic 4 (Nfatc4), which subsequently activates the expression of cleft lip and palate transmembrane protein 1-like protein (Clptm1l), a lipid scramblase involved in ferroptosis. Pharmacological and genetic inhibition of Erk5 in microglia effectively mitigates oxidative stress, lipid peroxidation, and ferroptosis, leading to a reduction in white matter damage and improved cognitive function. These findings underscore the potential of targeting the Erk5–Nfatc4–Clptm1l axis as a therapeutic strategy for ischemic white matter damage. Our study offers valuable insights into the molecular pathways driving white matter damage and provides a framework for the clinical translation of Erk5 inhibitors in the treatment of ischemic white matter damage.

Article Details

Volume / Issue Vol. 123, Issue 2
Published January 13, 2026
ISSN 0027-8424
Publisher National Academy of Sciences

Authors (18)

Y

Yun-Hui Chu

Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology

L

Lu-Yang Zhang

Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology

J

Jia-Yi He

Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology

Y

Ya-Fang Wang

Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology

M

Ming-Hao Dong

Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology

Y

Yun-Fan You

Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology

X

Xiao-Wei Pang

Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology

L

Li-Fang Zhu

Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology

H

Hang Zhang

L

Lu-Lu Xu

Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology

L

Lian Chen

L

Luo-Qi Zhou

Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology

J

Jun Xiao

K

Ke Shang

Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology

J

Jian-Ke Gong

College of Life Science and Technology, Key Laboratory of Molecular Biophysics of Ministry of Education, Huazhong University of Science and Technology

W

Wei Wang

D

Dai-Shi Tian

Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology

C

Chuan Qin

Department of Neurology, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology