Milan K L, Megha Bhatnagar, Ramkumar K M
Department of Biotechnology, School of Bioengineering, SRM Institute of Science and Technology, Kattankulathur, 603 203, Tamil Nadu, India.
Mol Biol Rep. 2025 Jun 21;52(1):621. doi: 10.1007/s11033-025-10719-5.
Diabetes mellitus (DM) is a chronic metabolic disease characterized by insulin resistance and hyperglycemia. Emerging evidence suggests that chronic inflammation is central to the development of diabetes and associated complications. Inflammasomes, multi-protein complexes, are key regulators of the innate immune response. The pro-inflammatory cytokines such as interleukin-1β (IL-1β) and interleukin-18 (IL-18) are released upon activation. This causes inflammation in DM. This review aims to explain the mechanisms leading to the activation of inflammasomes and the regulation of different inflammasome isoforms concerning DM and related complications such as cardiovascular disease, neuropathy, nephropathy, and retinopathy. We will also explore the impact of metabolic factors like hyperglycemia and insulin resistance on activating inflammasomes. A better understanding of the interplay between different inflammasome isoforms and DM can help develop novel therapeutic strategies that target inflammasome pathways for preventing and treating complications associated with diabetes.
糖尿病（DM）是一种以胰岛素抵抗和高血糖为特征的慢性代谢性疾病。新出现的证据表明，慢性炎症是糖尿病及其相关并发症发生发展的核心。炎性小体是多蛋白复合物，是先天免疫反应的关键调节因子。促炎细胞因子如白细胞介素-1β（IL-1β）和白细胞介素-18（IL-18）在激活后释放。这会导致糖尿病中的炎症。本综述旨在解释导致炎性小体激活的机制以及与糖尿病和相关并发症（如心血管疾病、神经病变、肾病和视网膜病变）相关的不同炎性小体亚型的调节。我们还将探讨高血糖和胰岛素抵抗等代谢因素对激活炎性小体的影响。更好地理解不同炎性小体亚型与糖尿病之间的相互作用有助于开发针对炎性小体途径的新型治疗策略，以预防和治疗与糖尿病相关的并发症。
