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Swollen Feet: Considering the Paradoxical Roles of Interleukins in Nephrotic Syndrome.
Kovalik, Maria E; Dacanay, Monique A; Crowley, Steven D; Hall, Gentzon.
Afiliación
  • Kovalik ME; Division of Nephrology, Duke University, Durham, NC 27701, USA.
  • Dacanay MA; Duke Molecular Physiology Institute, Duke University, Durham, NC 27710, USA.
  • Crowley SD; Division of Nephrology, Duke University, Durham, NC 27701, USA.
  • Hall G; Duke Molecular Physiology Institute, Duke University, Durham, NC 27710, USA.
Biomedicines ; 12(4)2024 Mar 26.
Article en En | MEDLINE | ID: mdl-38672094
ABSTRACT
Interleukins are a family of 40 bioactive peptides that act through cell surface receptors to induce a variety of intracellular responses. While interleukins are most commonly associated with destructive, pro-inflammatory signaling in cells, some also play a role in promoting cellular resilience and survival. This review will highlight recent evidence of the cytoprotective actions of the interleukin 1 receptor (IL-1R)- and common gamma chain receptor (IL-Rγc)-signaling cytokines in nephrotic syndrome (NS). NS results from the injury or loss of glomerular visceral epithelial cells (i.e., podocytes). Although the causes of podocyte dysfunction vary, it is clear that pro-inflammatory cytokines play a significant role in regulating the propagation, duration and severity of disease. Pro-inflammatory cytokines signaling through IL-1R and IL-Rγc have been shown to exert anti-apoptotic effects in podocytes through the phosphoinositol-3-kinase (PI-3K)/AKT pathway, highlighting the potential utility of IL-1R- and IL-Rγc-signaling interleukins for the treatment of podocytopathy in NS. The paradoxical role of interleukins as drivers and mitigators of podocyte injury is complex and ill-defined. Emerging evidence of the cytoprotective role of some interleukins in NS highlights the urgent need for a nuanced understanding of their pro-survival benefits and reveals their potential as podocyte-sparing therapeutics for NS.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Biomedicines Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Biomedicines Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza