Chang Shuye, Wang Zhaohui, An Tianhui
Department of Geriatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Biomedicines. 2024 Aug 14;12(8):1844. doi: 10.3390/biomedicines12081844.
Atherosclerosis is a key pathological basis for cardiovascular diseases, significantly influenced by T-cell-mediated immune responses. T-cells differentiate into various subtypes, such as pro-inflammatory Th1/Th17 and anti-inflammatory Th2/Treg cells. The imbalance between these subtypes is critical for the progression of atherosclerosis (AS). Recent studies indicate that metabolic reprogramming within various microenvironments can shift T-cell differentiation towards pro-inflammatory or anti-inflammatory phenotypes, thus influencing AS progression. This review examines the roles of pro-inflammatory and anti-inflammatory T-cells in atherosclerosis, focusing on how their metabolic reprogramming regulates AS progression and the associated molecular mechanisms of mTOR and AMPK signaling pathways.
动脉粥样硬化是心血管疾病的关键病理基础,受T细胞介导的免疫反应影响显著。T细胞可分化为多种亚型,如促炎性Th1/Th17细胞和抗炎性Th2/Treg细胞。这些亚型之间的失衡对动脉粥样硬化(AS)的进展至关重要。最近的研究表明,各种微环境中的代谢重编程可使T细胞分化向促炎或抗炎表型转变,从而影响AS进展。本综述探讨促炎性和抗炎性T细胞在动脉粥样硬化中的作用,重点关注其代谢重编程如何调节AS进展以及mTOR和AMPK信号通路的相关分子机制。