RIPK3 and kidney disease

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

doi:10.1016/j.nefro.2022.12.009

Cited by 2 publications

(1 citation statement)

References 92 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, additional canonical and non-canonical pathways for RIPK3 activation exist that do not require RIPK1 63 , 64 (Fig. 3c ); moreover, RIPK3 can promote inflammatory responses independent of necroptosis 65 , 66 . In kidney cells, inhibition of caspases prevents apoptosis, but may lead to RIPK1-mediated necroptosis, as observed in a model of cytokine-induced tubule cell death 18 , 67 .…”

Section: Regulated Necrosismentioning

confidence: 99%

Regulated cell death pathways in kidney disease

et al. 2023

Self Cite

View full text Add to dashboard Cite

Disorders of cell number that result from an imbalance between the death of parenchymal cells and the proliferation or recruitment of maladaptive cells contributes to the pathogenesis of kidney disease. Acute kidney injury can result from an acute loss of kidney epithelial cells. In chronic kidney disease, loss of kidney epithelial cells leads to glomerulosclerosis and tubular atrophy, whereas interstitial inflammation and fibrosis result from an excess of leukocytes and myofibroblasts. Other conditions, such as acquired cystic disease and kidney cancer, are characterized by excess numbers of cyst wall and malignant cells, respectively. Cell death modalities act to clear unwanted cells, but disproportionate responses can contribute to the detrimental loss of kidney cells. Indeed, pathways of regulated cell death — including apoptosis and necrosis — have emerged as central events in the pathogenesis of various kidney diseases that may be amenable to therapeutic intervention. Modes of regulated necrosis, such as ferroptosis, necroptosis and pyroptosis may cause kidney injury directly or through the recruitment of immune cells and stimulation of inflammatory responses. Importantly, multiple layers of interconnections exist between different modalities of regulated cell death, including shared triggers, molecular components and protective mechanisms.

show abstract

Section: Regulated Necrosismentioning

confidence: 99%

Regulated cell death pathways in kidney disease

et al. 2023

Self Cite

View full text Add to dashboard Cite

show abstract

RIPK3 signaling and its role in regulated cell death and diseases

Zhou,

Xiang,

Liu

et al. 2024

Cell Death Discov.

View full text Add to dashboard Cite

Receptor-interacting protein kinase 3 (RIPK3), a member of the receptor-interacting protein kinase (RIPK) family with serine/threonine protein kinase activity, interacts with RIPK1 to generate necrosomes, which trigger caspase-independent programmed necrosis. As a vital component of necrosomes, RIPK3 plays an indispensable role in necroptosis, which is crucial for human life and health. In addition, RIPK3 participates in the pathological process of several infections, aseptic inflammatory diseases, and tumors (including tumor-promoting and -suppressive activities) by regulating autophagy, cell proliferation, and the metabolism and production of chemokines/cytokines. This review summarizes the recent research progress of the regulators of the RIPK3 signaling pathway and discusses the potential role of RIPK3/necroptosis in the aetiopathogenesis of various diseases. An in-depth understanding of the mechanisms and functions of RIPK3 may facilitate the development of novel therapeutic strategies.

show abstract

RIPK3 and kidney disease

Cited by 2 publications

References 92 publications

Regulated cell death pathways in kidney disease

Regulated cell death pathways in kidney disease

RIPK3 signaling and its role in regulated cell death and diseases

Contact Info

Product

Resources

About