Karamitsos Konstantinos, Oikonomou Evangelos, Theofilis Panagiotis, Ikonomidis Ignatios, Kassi Eva, Lambadiari Vaia, Gialafos Elias, Tsatsaragkou Aikaterini, Mystakidi Vasiliki-Chara, Zisimos Konstantinos, Dimitriadis Kyriakos, Tousoulis Dimitris, Siasos Gerasimos
3rd Department of Cardiology, Sotiria Chest Disease Hospital, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece.
1st Department of Cardiology, Hippokration General Hospital, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece.
J Clin Med. 2025 Jun 29;14(13):4606. doi: 10.3390/jcm14134606.
Diabetes Mellitus (DM) is among the most common non-infectious causes of death globally, with Type 2 DM (T2DM) representing the majority of cases. T2DM is primarily characterized by insulin resistance, leading to hyperglycemia and compensatory hyperinsulinemia. Rapid changes in lifestyle, technological advancement, and societal evolution have fueled a global rise in T2DM, making it a major public health concern. The condition is associated with numerous complications-both macrovascular and microvascular-including coronary artery disease, heart failure, chronic kidney disease, and diabetic retinopathy, all of which contribute to increased morbidity and early mortality. Chronic tissue inflammation is now recognized as a key factor in the development of T2DM, with elevated inflammatory markers serving as predictors of the disease. In particular, the NLRP3 inflammasome complex has emerged as a central player in this inflammatory process. NLRP3 acts as an intracellular sensor for danger signals and tissue injury, triggering inflammatory responses and contributing to endothelial dysfunction and T2DM pathogenesis. Its role in linking metabolic stress to inflammation has positioned it as a promising therapeutic target. This review focuses on the mechanisms underlying NLRP3 inflammasome activation and its role in T2DM and related vascular complications. Additionally, it highlights emerging therapies that target NLRP3, offering new potential strategies for the prevention and treatment of T2DM.
糖尿病（DM）是全球最常见的非传染性死亡原因之一，其中2型糖尿病（T2DM）占大多数病例。T2DM的主要特征是胰岛素抵抗，导致高血糖和代偿性高胰岛素血症。生活方式的快速变化、技术进步和社会演变推动了全球T2DM发病率的上升，使其成为一个主要的公共卫生问题。该疾病与多种大血管和微血管并发症相关，包括冠状动脉疾病、心力衰竭、慢性肾病和糖尿病视网膜病变，所有这些都会导致发病率增加和早期死亡。慢性组织炎症现在被认为是T2DM发病的关键因素，炎症标志物升高可作为该疾病的预测指标。特别是，NLRP3炎性小体复合物已成为这一炎症过程的核心参与者。NLRP3作为危险信号和组织损伤的细胞内传感器，触发炎症反应，并导致内皮功能障碍和T2DM发病机制。它在将代谢应激与炎症联系起来的作用使其成为一个有前景的治疗靶点。本综述重点关注NLRP3炎性小体激活的潜在机制及其在T2DM和相关血管并发症中的作用。此外，它还强调了针对NLRP3的新兴疗法，为T2DM的预防和治疗提供了新的潜在策略。
