Molecular mechanisms of trauma-induced acute kidney injury: Inflammatory and metabolic insights from animal models.
Biochim Biophys Acta Mol Basis Dis
; 1863(10 Pt B): 2661-2671, 2017 10.
Article
em En
| MEDLINE
| ID: mdl-28431991
ABSTRACT
Trauma-induced acute kidney injury (AKI), such as after hemorrhagic shock (HS) or burn, remains a significant problem in the intensive care unit and is associated with increased mortality. The pathophysiology that drives AKI post-trauma is multi-factorial, and includes both inflammatory and metabolic alterations. Identifying the systemic profile that contributes to AKI is crucial not only for early diagnosis, but also for identifying treatments that improve kidney function and maintaining long-term patient health. In an effort to elucidate this molecular pathophysiology researchers have utilized a variety of animal models including chemically-induced (i.e., cisplatin), blocking renal perfusion (i.e., arterial clamping) and inducing burn or HS. As the latter burn and HS models are unequivocally applicable to studying AKI in the context of traumatic injury, this review will summarize the inflammatory and metabolic insights associated with AKI gained with these animal models. Moreover, novel therapeutic strategies brought forth with these models will be discussed.
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Ferimentos e Lesões
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Modelos Animais de Doenças
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Injúria Renal Aguda
Tipo de estudo:
Diagnostic_studies
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Etiology_studies
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Prognostic_studies
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Screening_studies
Limite:
Animals
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Humans
Idioma:
En
Revista:
Biochim Biophys Acta Mol Basis Dis
Ano de publicação:
2017
Tipo de documento:
Article