BET inhibitor nanotherapy halts kidney damage and reduces chronic kidney disease progression after ischemia-reperfusion injury

Targeting epigenetic mechanisms has emerged as a potential therapeutic approach for the treatment of kidney diseases. Specifically, inhibiting the bromodomain and extra-terminal (BET) domain proteins using the small molecule inhibitor JQ1 has shown promise in preclinical models of acute kidney injur...

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Veröffentlicht in:	Biomedicine & pharmacotherapy 2024-05, Vol.174, p.116492-116492, Article 116492
Hauptverfasser:	Saiz, Maria Laura, Lozano-Chamizo, Laura, Florez, Aida Bernardo, Marciello, Marzia, Diaz-Bulnes, Paula, Corte-Iglesias, Viviana, Bernet, Cristian Ruiz, Rodrigues-Diez, Raul R., Martin-Martin, Cristina, Rodriguez-Santamaria, Mar, Fernandez-Vega, Ivan, Rodriguez, Ramon M., Diaz-Corte, Carmen, Suarez-Alvarez, Beatriz, Filice, Marco, Lopez-Larrea, Carlos
Format:	Artikel
Sprache:	eng
Schlagworte:	Acute Kidney Injury - drug therapy Acute Kidney Injury - prevention & control AKI Animals Azepines - administration & dosage Azepines - pharmacology BRD4 Bromodomain Containing Proteins Cell Cycle Proteins - antagonists & inhibitors Disease Models, Animal Disease Progression ischemia reperfusion injury JQ1 Kidney - drug effects Kidney - metabolism Kidney - pathology kidney drug delivery Liposomes Male Mice Mice, Inbred C57BL nanobiotechnology Nanoparticles Nuclear Proteins Renal Insufficiency, Chronic - drug therapy Renal Insufficiency, Chronic - pathology Reperfusion Injury - drug therapy Reperfusion Injury - pathology Transcription Factors - antagonists & inhibitors Transcription Factors - metabolism Triazoles - administration & dosage Triazoles - pharmacology
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