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Background Chronic allograft dysfunction (CAD) represents a complex process of inflammatory response, fibrosis, and tissue restoration, mediated by a myriad of proinflammatory cytokines, enzymes, and growth factors. NOD-like receptor protein3 (NLRP3) inflammasome is one of the NLR protein families. It drives proteolysis of proinflammatory caspases which induces maturation of pro-interleukin (IL)-1β and pro-IL-18. The aim of this work is to study NLRP3 inflammasome activation in patients with renal transplantation in relation to allograft function, inflammation, and renal fibrosis.
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Aggan et al. (2024) studied this question.
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