Suppr超能文献

细胞焦亡与糖尿病创面愈合中的炎症小体

Pyroptosis and inflammasomes in diabetic wound healing.

机构信息

College of Pharmacy, Zunyi Medical University, Zunyi, China.

Key Laboratory of Basic Pharmacalogy of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi, China.

出版信息

Front Endocrinol (Lausanne). 2022 Aug 5;13:950798. doi: 10.3389/fendo.2022.950798. eCollection 2022.

Abstract

Diabetic wound is one of the complications of diabetes and is not easy to heal. It often evolves into chronic ulcers, and severe patients will face amputation. Compared with normal wounds, diabetic wounds have an increased proportion of pro-inflammatory cytokines that are detrimental to the normal healing response. The burden of this disease on patients and healthcare providers is overwhelming, and practical solutions for managing and treating diabetic wounds are urgently needed. Pyroptosis, an inflammatory type of programmed cell death, is usually triggered by the inflammasome. The pyroptosis-driven cell death process is primarily mediated by the traditional signaling pathway caused by caspase -1 and the non-classical signaling pathways induced by caspase -4/5/11. Growing evidence that pyroptosis promotes diabetic complications, including diabetic wounds. In addition, inflammation is thought to be detrimental to wound healing. It is worth noting that the activation of the NLRP3 inflammasome plays a crucial role in the recovery of diabetic wounds. This review has described the mechanisms of pyroptosis-related signaling pathways and their impact on diabetic wounds. It has discussed new theories and approaches to promote diabetic wound healing, as well as some potential compounds targeting pyroptosis and inflammasome signaling pathways that could be new approaches to treating diabetic wounds.

摘要

糖尿病性创面是糖尿病的并发症之一,不易愈合。它常演变为慢性溃疡,严重的患者将面临截肢。与正常创面相比,糖尿病性创面中促炎细胞因子的比例增加,不利于正常的愈合反应。这种疾病给患者和医疗保健提供者带来的负担是巨大的,迫切需要实用的方法来管理和治疗糖尿病性创面。细胞焦亡是一种炎症性的程序性细胞死亡,通常由炎性小体触发。细胞焦亡驱动的细胞死亡过程主要由半胱天冬酶-1 引起的传统信号通路和半胱天冬酶-4/5/11 诱导的非经典信号通路介导。越来越多的证据表明,细胞焦亡促进了糖尿病并发症的发生,包括糖尿病性创面。此外,炎症被认为不利于伤口愈合。值得注意的是,NLRP3 炎性小体的激活在糖尿病创面的恢复中起着至关重要的作用。本综述描述了与细胞焦亡相关的信号通路及其对糖尿病性创面的影响,探讨了促进糖尿病性创面愈合的新理论和方法,以及一些针对细胞焦亡和炎性小体信号通路的潜在化合物,这些可能为治疗糖尿病性创面提供新的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/09cf/9389066/1d9ba1939524/fendo-13-950798-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验