Gene deficiency or pharmacological inhibition of PDCD4-mediated FGR signaling protects against acute kidney injury
Acta Pharmaceutica Sinica B
; (6): 394-405, 2021.
Article
em En
| WPRIM
| ID: wpr-881143
Biblioteca responsável:
WPRO
ABSTRACT
Recent studies have shown that programmed cell death 4 (PDCD4) modulates distinct signal transduction pathways in different pathological conditions. Despite acute and chronic immune responses elicited by ischemia contributing to the functional deterioration of the kidney, the contributions and mechanisms of PDCD4 in acute kidney injury (AKI) have remained unclear. Using two murine AKI models including renal ischemia/reperfusion injury (IRI) and cisplatin-induced AKI, we found that PDCD4 deficiency markedly ameliorated renal dysfunction and inflammatory responses in AKI mice. Consistently, upregulation of PDCD4 was also confirmed in the kidneys from patients with biopsy confirmed acute tubular necrosis from a retrospective cohort study. Moreover, we found that overexpression of
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Índice:
WPRIM
Tipo de estudo:
Observational_studies
Idioma:
En
Revista:
Acta Pharmaceutica Sinica B
Ano de publicação:
2021
Tipo de documento:
Article