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RESEARCH PAPER / 2026-01-18

SRC suppression attenuates vascular aging by activating FUNDC1-dependent mitophagy.

Linghuan Wang, Yan Ma, Tianhu Wang, Weiwei Zhang, Zhiyi Fang, Tingting Lu, Yingjie Zhang, Yan Fang, Ting Sun, Dong Han, Feng Cao

Department of Medicine School, Nankai University, Tianjin 300071, China; Institute of Geriatric Medicine, National Clinical Research Centre for Geriatric Diseases, National Key Lab for Chronic Kidney Disease, Second Medical Centre of Chinese PLA General Hospital, Beijing 100853, China. · pubmed

Abstract

Vascular smooth muscle cell senescence contributes critically to vascular remodeling and atherosclerosis, with mitochondrial dysfunction and impaired mitophagy recognized as major contributors. SRC, a stress-responsive tyrosine kinase, has been linked to aging, yet its role in vascular aging remains unclear. Here, we examined the role of SRC in regulating autophagy/mitophagy using in vitro and in vivo models. An accelerated vascular aging model was established using a high-fat diet and streptozotocin injection in ApoE

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

SRC suppression activates FUNDC1-dependent mitophagy, which attenuates vascular aging. This research addresses the mechanisms underlying vascular aging, focusing on SRC's role in mitophagy, which is relevant to understanding and potentially mitigating the root causes of aging.

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