Platelet-derived microparticles induce CD8+ T cell senescence in chronic kidney disease via the transfer of microRNA-550a-5p
- 1Department of Nephrology, Chongqing Key Laboratory of Prevention and Treatment of Kidney Disease, Chongqing Clinical Research Center of Kidney and Urology Diseases, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037 China
- 2Department of Nephrology, General Hospital of Western Theater Command, PLA, Chengdu, China
- 3State Key Laboratory of Trauma and Chemical Poisoning, Institute of Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University (Third Military Medical University), Chongqing, 400038 China
Abstract
Infection is a leading cause of mortality in patients with chronic kidney disease (CKD), in which T cell dysfunction is considered a typical feature. Although platelets are active participants in immune response, their role in regulating T cell function in patients with CKD remains unclear. In this study, we demonstrate that CD8+ T cell senescence may be a major contributor to the immunosuppressed state of patients with CKD, and that platelets derived from patients with CKD can induce premature CD8+ T cell senescence, potentially through mediating mitochondrial dysfunction. Further investigations reveal that platelet-derived microparticles (PMPs) from patients with CKD promote CD8+ T cell senescence via transferring miR-550a-5p, thereby decreasing PMPCB expression and inducing NDUFS8 cleavage failure. Finally, inhibition of miR-550a-5p and pretreatment with nicotinamide mononucleotide are capable of preventing platelet-induced CD8+ T cell senescence in CKD patients. Collectively, these findings suggest that the ectopic transient expression of platelet-derived miR-550a-5p in CD8+ T cells promotes cellular senescence by regulating the PMPCB–NDUFS8 axis, which can be exploited to treat CKD-associated immunosenescence.
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BibTeX
@article{sun2026plateletderived,
title = {{Platelet-derived microparticles induce CD8+ T cell senescence in chronic kidney disease via the transfer of microRNA-550a-5p}},
author = {Yuewen Sun and Qigang Lan and Yaqin Wang and Minhua Xie and Xinyi Wu and Liangjing Lv and Qing Xin and Jun Chen and Xiaoyi Zhong and Mengying Yao and Shuiqin Gong and Siyan Zhou and Junping Wang and Jinghong Zhao},
journal = {Experimental and Molecular Medicine},
year = {2026},
month = oct,
doi = {10.1038/s12276-026-01876-z},
url = {https://doi.org/10.1038/s12276-026-01876-z},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Platelet-derived microparticles induce CD8+ T cell senescence in chronic kidney disease via the transfer of microRNA-550a-5p
AU - Yuewen Sun
AU - Qigang Lan
AU - Yaqin Wang
AU - Minhua Xie
AU - Xinyi Wu
AU - Liangjing Lv
AU - Qing Xin
AU - Jun Chen
AU - Xiaoyi Zhong
AU - Mengying Yao
AU - Shuiqin Gong
AU - Siyan Zhou
AU - Junping Wang
AU - Jinghong Zhao
PY - 2026
DA - 2026/10/01
JO - Experimental and Molecular Medicine
DO - 10.1038/s12276-026-01876-z
UR - https://doi.org/10.1038/s12276-026-01876-z
AB - Infection is a leading cause of mortality in patients with chronic kidney disease (CKD), in which T cell dysfunction is considered a typical feature. Although platelets are active participants in immune response, their role in regulating T cell function in patients with CKD remains unclear. In this study, we demonstrate that CD8+ T cell senescence may be a major contributor to the immunosuppressed state of patients with CKD, and that platelets derived from patients with CKD can induce premature CD8+ T cell senescence, potentially through mediating mitochondrial dysfunction. Further investigations reveal that platelet-derived microparticles (PMPs) from patients with CKD promote CD8+ T cell senescence via transferring miR-550a-5p, thereby decreasing PMPCB expression and inducing NDUFS8 cleavage failure. Finally, inhibition of miR-550a-5p and pretreatment with nicotinamide mononucleotide are capable of preventing platelet-induced CD8+ T cell senescence in CKD patients. Collectively, these findings suggest that the ectopic transient expression of platelet-derived miR-550a-5p in CD8+ T cells promotes cellular senescence by regulating the PMPCB–NDUFS8 axis, which can be exploited to treat CKD-associated immunosenescence.
SN - 2092-6413
SN - 1226-3613
ER -