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RIPK1 和 RIPK3 抑制剂:治疗糖尿病并发症的炎症治疗潜在武器。

RIPK1 and RIPK3 inhibitors: potential weapons against inflammation to treat diabetic complications.

机构信息

College of Life Sciences, Mudanjiang Medical University, Mudanjiang, China.

Heilongjiang Key Laboratory of Tissue Damage and Repair, Mudanjiang Medical University, Mudanjiang, China.

出版信息

Front Immunol. 2023 Oct 26;14:1274654. doi: 10.3389/fimmu.2023.1274654. eCollection 2023.

DOI:10.3389/fimmu.2023.1274654
PMID:37954576
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10639174/
Abstract

Diabetes mellitus is a metabolic disease that is characterized by chronic hyperglycemia due to a variety of etiological factors. Long-term metabolic stress induces harmful inflammation leading to chronic complications, mainly diabetic ophthalmopathy, diabetic cardiovascular complications and diabetic nephropathy. With diabetes complications being one of the leading causes of disability and death, the use of anti-inflammatories in combination therapy for diabetes is increasing. There has been increasing interest in targeting significant regulators of the inflammatory pathway, notably receptor-interacting serine/threonine-kinase-1 (RIPK1) and receptor-interacting serine/threonine-kinase-3 (RIPK3), as drug targets for managing inflammation in treating diabetes complications. In this review, we aim to provide an up-to-date summary of current research on the mechanism of action and drug development of RIPK1 and RIPK3, which are pivotal in chronic inflammation and immunity, in relation to diabetic complications which may be benefit for explicating the potential of selective RIPK1 and RIPK3 inhibitors as anti-inflammatory therapeutic agents for diabetic complications.

摘要

糖尿病是一种代谢性疾病,其特征是由于多种病因引起的慢性高血糖。长期的代谢应激导致有害的炎症反应,进而导致慢性并发症,主要包括糖尿病眼病、糖尿病心血管并发症和糖尿病肾病。由于糖尿病并发症是导致残疾和死亡的主要原因之一,因此在糖尿病的联合治疗中使用抗炎药的情况越来越多。人们越来越关注炎症途径的重要调节因子,特别是受体相互作用丝氨酸/苏氨酸激酶-1(RIPK1)和受体相互作用丝氨酸/苏氨酸激酶-3(RIPK3),将其作为治疗糖尿病并发症的抗炎药物靶点。在这篇综述中,我们旨在提供关于 RIPK1 和 RIPK3 的作用机制和药物开发的最新研究总结,这对于慢性炎症和免疫与糖尿病并发症之间的关系至关重要,这可能有助于阐明选择性 RIPK1 和 RIPK3 抑制剂作为治疗糖尿病并发症的抗炎治疗药物的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/471e/10639174/ba90e9638847/fimmu-14-1274654-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/471e/10639174/8c7a82c0b516/fimmu-14-1274654-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/471e/10639174/bc4f70fd86fd/fimmu-14-1274654-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/471e/10639174/ba90e9638847/fimmu-14-1274654-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/471e/10639174/8c7a82c0b516/fimmu-14-1274654-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/471e/10639174/bc4f70fd86fd/fimmu-14-1274654-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/471e/10639174/ba90e9638847/fimmu-14-1274654-g003.jpg

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High Glucose-Induced Kidney Injury via Activation of Necroptosis in Diabetic Kidney Disease.高糖诱导糖尿病肾病细胞发生坏死性凋亡导致肾损伤
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ADAR1 and ZBP1 in innate immunity, cell death, and disease.
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