Adult kidney explants is a physiologic model for studying diabetic nephropathy

Gómez-Jaramillo, Laura; Cano-Cano, Fátima; Campos‐Caro, Antonio; Alcalá, Martín; Álvarez-Gallego, Fabiola; Arroba, Ana I.; Aguilar‐Diosdado, Manuel

doi:10.1016/j.lfs.2022.120575

Cited by 2 publications

(2 citation statements)

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“…The BB rat develops diabetes spontaneously at 11 weeks old; however, it shows inflammatory progress from 7 weeks of age [ 38 ]. Recently, we have reported that BB rats present important inflammatory events prior to hyperglycemia or preclinical diabetic status [ 39 ]. As is shown in Figure 7 A, AK explants from BB rats at 7 weeks old, with euglycemic values in the blood, present increased levels of iNOS protein and mRNA expression that were significantly reduced in the presence of ( S S )-DS-ONJ.…”

Section: Resultsmentioning

confidence: 99%

“…In this way, it has been established that before suffering elevated blood glucose levels due to pancreatic failure, the kidney is being affected by the inflammatory phenomenon. The characterization of MCT cells as an in vitro model for studying the early events of DN has contributed to dissecting the signaling pathways involved in this pathology and the possible protective role of ( S S )-DS-ONJ on DN progression [ 39 ]. Further, the use of AK explants as a pathophysiological ex vivo model in DN has been relevant to testing therapeutic approaches.…”

Section: Discussionmentioning

confidence: 99%

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Unravelling the Inflammatory Processes in the Early Stages of Diabetic Nephropathy and the Potential Effect of (Ss)-DS-ONJ

Gómez-Jaramillo

Cano-Cano

Sánchez-Fernández

et al. 2022

IJMS

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Inflammatory processes play a central role in the pathogenesis of diabetic nephropathy (DN) in the early stages of the disease. The authors demonstrate that the glycolipid mimetic (Ss)-DS-ONJ is able to abolish inflammation via the induction of autophagy flux and provokes the inhibition of inflammasome complex in ex vivo and in vitro models, using adult kidney explants from BB rats. The contribution of (Ss)-DS-ONJ to reducing inflammatory events is mediated by the inhibition of classical stress kinase pathways and the blocking of inflammasome complex activation. The (Ss)-DS-ONJ treatment is able to inhibit the epithelial-to-mesenchymal transition (EMT) progression, but only when the IL18 levels are reduced by the treatment. These findings suggest that (Ss)-DS-ONJ could be a novel, and multifactorial treatment for DN.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%