Review
Version 1
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Type I IFN in Glomerular Disease: Scarring beyond the STING
Version 1
: Received: 1 January 2024 / Approved: 3 January 2024 / Online: 3 January 2024 (10:05:24 CET)
A peer-reviewed article of this Preprint also exists.
Jimenez-Uribe, A.P.; Mangos, S.; Hahm, E. Type I IFN in Glomerular Disease: Scarring beyond the STING. Int. J. Mol. Sci. 2024, 25, 2497. Jimenez-Uribe, A.P.; Mangos, S.; Hahm, E. Type I IFN in Glomerular Disease: Scarring beyond the STING. Int. J. Mol. Sci. 2024, 25, 2497.
Abstract
The field of nephrology has recently directed a considerable amount of attention towards the stimulator of interferon genes (STING) molecule since it appears to be a potent driver of chronic kidney disease (CKD). STING and its activator, the cyclic GMP-AMP synthase (cGAS) are among the most relevant inducers that promote the expression of type I interferons (IFN-Is). These cytokines have been long recognized as part of the mechanism used by the innate immune system to battle viral infections; however, their involvement in sterile inflammation remains unclear. Mounting evidence pointing to the involvement of the IFN-I pathway in sterile kidney inflammation provides potential insights into the complex interplay between the innate immune system and damage to the most sensitive segment of the nephron, the glomerulus. The STING pathway is often cited as the cause of renal disease originating from non-infection related caused by the induction of IFN-I expression. However, other receptors have been implicated in this process, mainly by recognizing host-derived nucleic acids. This review explores the main endogenous inducers of IFN-I in glomerular cells, discusses what exposure to the main autocrine and paracrine cytokines has on these cells, and identifies the pathways that are implicated in the development of glomerular damage.
Keywords
Glomerulonephritis; IFN-I pathway; Intracellular Pattern-Recognition Receptors; STING; sterile inflammation
Subject
Medicine and Pharmacology, Urology and Nephrology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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