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CCL11(嗜酸性粒细胞趋化因子)促进衰老相关心血管疾病的进展。

CCL11 (Eotaxin) Promotes the Advancement of Aging-Related Cardiovascular Diseases.

作者信息

Zhang Tanwei, Huang Yanhong, Ji Xinmeng, Wu Teng, Xiao Pingxi

机构信息

Key Laboratory of Targeted Intervention of Cardiovascular Disease and Collaborative Innovation Center for Cardiovascular Translational Medicine, Department of Pathophysiology, Nanjing Medical University, 211166 Nanjing, Jiangsu, China.

Department of Cardiology, The Fourth Affiliated Hospital of Nanjing Medical University, 210031 Nanjing, Jiangsu, China.

出版信息

Rev Cardiovasc Med. 2025 Feb 13;26(2):26020. doi: 10.31083/RCM26020. eCollection 2025 Feb.

Abstract

Aging-related diseases, such as cardiovascular diseases (CVDs), neurodegeneration, cancer, etc., have become important factors that threaten the lifespans of older individuals. A chronic inflammatory response is closely related to aging-related diseases. Establishing inflammatory aging clock (iAGE, deep-learning methods on blood immune biomarkers to construct a metric for age-related chronic inflammation) successfully predicted the positive correlation between several factors, including serum C-C-motif chemokine ligand 11 (CCL11) and aging-related diseases. Recently, the role and mechanism of CCL11, an eosinophilic chemokine, in neurodegenerative diseases have been widely reported. Additionally, many research studies have shown a positive correlation with CVDs, but the underlying mechanism remains unknown. This review focuses on the relationship between chronic inflammation and aging. The role of CCL11 will be discussed and summarized in relation to aging-related diseases, especially CVDs.

摘要

衰老相关疾病,如心血管疾病(CVD)、神经退行性变、癌症等,已成为威胁老年人寿命的重要因素。慢性炎症反应与衰老相关疾病密切相关。建立炎症衰老时钟(iAGE,一种基于血液免疫生物标志物的深度学习方法,用于构建与年龄相关的慢性炎症指标)成功预测了包括血清C-C基序趋化因子配体11(CCL11)在内的多个因素与衰老相关疾病之间的正相关关系。最近,嗜酸性粒细胞趋化因子CCL11在神经退行性疾病中的作用和机制已有广泛报道。此外,许多研究表明其与心血管疾病呈正相关,但其潜在机制仍不清楚。本综述重点关注慢性炎症与衰老之间的关系。将讨论并总结CCL11在衰老相关疾病,尤其是心血管疾病中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cfe4/11868897/ff05552318c6/2153-8174-26-2-26020-g1.jpg

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