RIPK3 and kidney disease

Guerrero-Mauvecin, Juan; Fontecha‐Barriuso, Miguel; Lopez-Díaz, Ana M; Ortíz, Alberto; Sanz, Ana B.

doi:10.1016/j.nefroe.2023.04.006

Cited by 1 publication

(2 citation statements)

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“…These results support the need to develop novel RIPK3 inhibitors as anti-inflammatory drugs to treat kidney disease. However, the knowledge gap that must be addressed is understanding the conformational changes in RIPK3 that trigger apoptosis [ 19 ] to develop better RIPK3 pharmacological inhibitors.…”

Section: Discussionmentioning

confidence: 99%

“…Necroptosis is initiated by the phosphorylation of receptor-interacting protein kinase-3 (RIPK3) by RIPK1 followed by RIPK3 phosphorylated mixed-lineage kinase domain-like protein (MLKL) phosphorylation, which leads to disruption of the plasma membrane [ 14 , 15 , 16 , 17 , 18 ]. However, RIPK3 can also mediate inflammation and/or fibrosis in the kidney independent of cell death, as it has been observed in different experimental models [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

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CCN2 Activates RIPK3, NLRP3 Inflammasome, and NRF2/Oxidative Pathways Linked to Kidney Inflammation

Rayego-Mateos,

Marquez-Exposito,

Basantes

et al. 2023

Antioxidants

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Inflammation is a key characteristic of both acute and chronic kidney diseases. Preclinical data suggest the involvement of the NLRP3/Inflammasome, receptor-interacting protein kinase-3 (RIPK3), and NRF2/oxidative pathways in the regulation of kidney inflammation. Cellular communication network factor 2 (CCN2, also called CTGF in the past) is an established fibrotic biomarker and a well-known mediator of kidney damage. CCN2 was shown to be involved in kidney damage through the regulation of proinflammatory and profibrotic responses. However, to date, the potential role of the NLRP3/RIPK3/NRF2 pathways in CCN2 actions has not been evaluated. In experimental acute kidney injury induced with folic acid in mice, CCN2 deficiency diminished renal inflammatory cell infiltration (monocytes/macrophages and T lymphocytes) as well as the upregulation of proinflammatory genes and the activation of NLRP3/Inflammasome-related components and specific cytokine products, such as IL-1β. Moreover, the NRF2/oxidative pathway was deregulated. Systemic administration of CCN2 to C57BL/6 mice induced kidney immune cell infiltration and activated the NLRP3 pathway. RIPK3 deficiency diminished the CCN2-induced renal upregulation of proinflammatory mediators and prevented NLRP3 modulation. These data suggest that CCN2 plays a fundamental role in sterile inflammation and acute kidney injury by modulating the RIKP3/NLRP3/NRF2 inflammatory pathways.

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Section: Discussionmentioning

confidence: 99%