Legumain deficiency halts atherogenesis by modulating T cell receptor signaling.

Xuying Xiang, Feng Zhang, Lei Nie, Xiaoqing Guo, Mengting Qin, Jiaojiao Chen, Dailiang Jiang, Zhentao Zhang, Ling Mao

Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. · pubmed

Paper

Abstract

Atherosclerosis is an age-related pathological process associated with elevated levels of legumain in plaques and plasma. However, the underlying mechanisms remain unclear. The aim of this study was to investigate the role of legumain in the progression of atherosclerotic plaques, with a particular focus on functional and phenotypic changes in CD4

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper investigates the role of legumain in atherosclerosis, which is an age-related disease. However, it primarily focuses on the mechanisms of atherogenesis rather than addressing the root causes of aging or lifespan extension. While it contributes to understanding a specific aspect of age-related pathology, its impact on the broader field of longevity research is limited.

Author of this paper? Send a correction.