Bruton's tyrosine kinase regulates macrophageinduced inflammation in the diabetic kidney via NLRP3 inflammasome activation.
Int J Mol Med
; 48(3)2021 Sep.
Article
en En
| MEDLINE
| ID: mdl-34278465
ABSTRACT
It has been previously reported that macrophages may be involved in diabetic nephropathy (DN) development. Furthermore, Bruton's tyrosine kinase (BTK) may participate in macrophage activation and lead to the release of inflammatory mediators. The main aim of the present study was to analyze the association between renal BTK expression and clinical indicators. Moreover, BTK knockout mice were used to establish a diabetic model for further research. The results demonstrated that BTK was activated in the kidneys of patients with DN and was associated with the progression of proteinuria, creatinine levels, estimated glomerular filtration rate and pathological changes in the kidneys of patients with DN. Furthermore, BTK knockout was observed to reduce urinary protein excretion, alleviate renal injury and decrease renal inflammation in diabetic mice. This protection may be attributed to BTKinduced suppression of the activation of the Nodlike receptor (NLR) family pyrin domain containing 3 inflammasome. Collectively, it has been demonstrated in the present study that BTK may be a potential target for DN treatment.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Diabetes Mellitus Experimental
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Nefropatías Diabéticas
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Proteína con Dominio Pirina 3 de la Familia NLR
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Agammaglobulinemia Tirosina Quinasa
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Inflamación
Tipo de estudio:
Etiology_studies
Límite:
Animals
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Humans
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Male
Idioma:
En
Revista:
Int J Mol Med
Asunto de la revista:
BIOLOGIA MOLECULAR
/
GENETICA MEDICA
Año:
2021
Tipo del documento:
Article