Inflammation in cardiovascular-kidney-metabolic syndrome: key roles and underlying mechanisms-a comprehensive review.

IF 3.7 2区 生物学 Q3 CELL BIOLOGY
Zhen Xu, Shuo Yang, Yuan Tan, Qian Zhang, He Wang, Jingjin Tao, Qi Liu, Qingchen Wang, Weimin Feng, Zhongxin Li, Chong Wang, Liyan Cui
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引用次数: 0

Abstract

Cardiovascular-Kidney-Metabolic (CKM) syndrome, a newly defined systemic disorder, is characterized by the pathological interplay among diabetes, chronic kidney disease (CKD), and cardiovascular disease (CVD). Recent studies have identified chronic inflammation not only as a central mediator in the pathological progression of CKM syndrome but also as a pivotal molecular hub that drives coordinated damage across multiple organ systems. Mechanistic investigations have revealed that aberrant activation of signaling pathways such as NF-κB, Wnt, PI3K-AKT, JAK-STAT, and PPAR constitutes a complex inflammatory regulatory network. Notably, these pathways facilitate inter-organ inflammatory crosstalk, establishing positive feedback loops among the heart, kidneys, and metabolic tissues. This, in turn, amplifies pathological processes such as oxidative stress, endothelial dysfunction, and fibrosis in a cascading manner.This review systematically delineates the multidimensional pathophysiological mechanisms of CKM syndrome, with particular emphasis on the inter-organ inflammatory regulation mediated by key signaling pathways. Furthermore, we explore the translational potential of therapeutic strategies targeting inflammatory cytokines (e.g., IL-1β, IL-6, and TNF-α) based on the latest clinical evidence, aiming to provide a theoretical framework and novel perspectives for disrupting the vicious cycle of CKM syndrome.

心血管-肾-代谢综合征中的炎症:关键作用和潜在机制综述
心血管-肾代谢综合征(CKM)是一种新定义的全身性疾病,其特点是糖尿病、慢性肾脏疾病(CKD)和心血管疾病(CVD)之间的病理相互作用。最近的研究发现,慢性炎症不仅是CKM综合征病理进展的中心介质,而且是驱动多器官系统协调损伤的关键分子枢纽。机制研究表明,NF-κB、Wnt、PI3K-AKT、JAK-STAT和PPAR等信号通路的异常激活构成了一个复杂的炎症调节网络。值得注意的是,这些途径促进了器官间的炎症串扰,在心脏、肾脏和代谢组织之间建立了正反馈回路。这反过来又以级联方式放大了诸如氧化应激、内皮功能障碍和纤维化等病理过程。本文系统地阐述了CKM综合征的多维病理生理机制,特别强调了关键信号通路介导的器官间炎症调节。此外,我们基于最新的临床证据,探索针对炎症细胞因子(如IL-1β、IL-6和TNF-α)的治疗策略的转化潜力,旨在为破坏CKM综合征的恶性循环提供理论框架和新视角。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Molecular and Cellular Biochemistry
Molecular and Cellular Biochemistry 生物-细胞生物学
CiteScore
8.30
自引率
2.30%
发文量
293
审稿时长
1.7 months
期刊介绍: Molecular and Cellular Biochemistry: An International Journal for Chemical Biology in Health and Disease publishes original research papers and short communications in all areas of the biochemical sciences, emphasizing novel findings relevant to the biochemical basis of cellular function and disease processes, as well as the mechanics of action of hormones and chemical agents. Coverage includes membrane transport, receptor mechanism, immune response, secretory processes, and cytoskeletal function, as well as biochemical structure-function relationships in the cell. In addition to the reports of original research, the journal publishes state of the art reviews. Specific subjects covered by Molecular and Cellular Biochemistry include cellular metabolism, cellular pathophysiology, enzymology, ion transport, lipid biochemistry, membrane biochemistry, molecular biology, nuclear structure and function, and protein chemistry.
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