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

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FRONTIERS IN IMMUNOLOGY
卷 14, 期 -, 页码 -

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FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2023.1274654

关键词

diabetes; diabetic complications; inflammation; regulatory cell death; receptor interacting protein kinase

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Diabetes is a metabolic disease that causes chronic high blood sugar, leading to harmful inflammation and complications. Anti-inflammatory drugs, specifically targeting RIPK1 and RIPK3, have shown potential in managing inflammation and treating diabetes complications. This review provides a summary of the current research on the mechanism of action and drug development of RIPK1 and RIPK3.
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.

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