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. 2018 Feb 20;9:114. doi: 10.3389/fphys.2018.00114

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Copyright © 2018 Sharma, Tate, Mathew, Vince, Ritchie and de Haan.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The role of the NLRP3 inflammasome and interconnectivity with oxidative stress and inflammation in the development of complications in diabetes. Metabolic changes in diabetes including insulin resistance, hyperlipidaemia and hyperglycaemia (and the subsequent production of DAMPs), lead to an increase in inflammation, oxidative stress and NLRP3 inflammasome activation and subsequent development of diabetic complications including diabetic nephropathy, atherosclerosis, diabetic cardiomyopathy, diabetic neuropathy and diabetic retinopathy. DAMPs, damage associated molecular patterns; RAGE, receptor for advanced glycation end-products; IAPP, islet amyloid polypeptide protein.