NLRP3 Inflammasome: A central player in renal pathologies and nephropathy.

Autor: Henedak NT; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Ahram Canadian University, 6(th) of October City, Giza, Egypt., El-Abhar HS; Department of Pharmacology, Toxicology, and Biochemistry, Faculty of Pharmacy, Future University in Egypt, Cairo 11835, Egypt., Soubh AA; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Ahram Canadian University, 6(th) of October City, Giza, Egypt., Abdallah DM; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt. Electronic address: dalaal.abdallah@pharma.cu.edu.eg.
Jazyk: angličtina
Zdroj: Life sciences [Life Sci] 2024 Aug 15; Vol. 351, pp. 122813. Date of Electronic Publication: 2024 Jun 08.
DOI: 10.1016/j.lfs.2024.122813
Abstrakt: The cytoplasmic oligomer NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome has been implicated in most inflammatory and autoimmune diseases. Here, we highlight the significance of NLRP3 in diverse renal disorders, demonstrating its activation in macrophages and non-immune tubular epithelial and mesangial cells in response to various stimuli. This activation leads to the release of pro-inflammatory cytokines, contributing to the development of acute kidney injury (AKI), chronic renal injury, or fibrosis. In AKI, NLRP3 inflammasome activation and pyroptotic renal tubular cell death is driven by contrast and chemotherapeutic agents, sepsis, and rhabdomyolysis. Nevertheless, inflammasome is provoked in disorders such as crystal and diabetic nephropathy, obesity-related renal fibrosis, lupus nephritis, and hypertension-induced renal damage that induce chronic kidney injury and/or fibrosis. The mechanisms by which the inflammatory NLRP3/ Apoptosis-associated Speck-like protein containing a Caspase recruitment domain (ASC)/caspase-1/interleukin (IL)-1β & IL-18 pathway can turn on renal fibrosis is also comprehended. This review further outlines the involvement of dopamine and its associated G protein-coupled receptors (GPCRs), including D1-like (D1, D5) and D2-like (D2-D4) subtypes, in regulating this inflammation-linked renal dysfunction pathway. Hence, we identify D-related receptors as promising targets for renal disease management by inhibiting the functionality of the NLRP3 inflammasome.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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