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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)


Texto completo
Goncalves, Giselle Martins ; Zamboni, Dario S. [1] ; Saraiva Camara, Niels Olsen [2]
Número total de Autores: 3
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Med Sch Ribeirao Preto, Dept Cell Biol, BR-05508900 Sao Paulo - Brazil
[2] Univ Sao Paulo, Med Sch Ribeirao Preto, Dept Immunol, Lab Transplantat Immunobiol, Inst Biomed Sci 4, BR-05508900 Sao Paulo - Brazil
Número total de Afiliações: 2
Tipo de documento: Artigo Científico
Fonte: Shock; v. 34, n. 1, p. 22-26, SEP 2010.
Citações Web of Science: 43

Acute kidney injury (AKI) is an important clinical syndrome characterized by abnormalities in the hydroelectrolytic balance. Because of high rates of morbidity and mortality (from 15% to 60%) associated with AKI, the study of its pathophysiology is critical in searching for clinical targets and therapeutic strategies. Severe sepsis is the major cause of AKI. The host response to sepsis involves an inflammatory response, whereby the pathogen is initially sensed by innate immune receptors (pattern recognition receptors {[}PRRs]). When it persists, this immune response leads to secretion of proinflammatory products that induce organ dysfunction such as renal failure and consequently increased mortality. Moreover, the injured tissue releases molecules resulting from extracellular matrix degradation or dying cells that function as alarmines, which are recognized by PRR in the absence of pathogens in a second wave of injury. Toll-like receptors (TLRs) and NOD-like receptors (NLRs) are the best characterized PRRs. They are expressed in many cell types and throughout the nephron. Their activation leads to translocation of nuclear factors and synthesis of proinflammatory cytokines and chemokines. TLRs' signaling primes the cells for a robust inflammatory response dependent on NLRs; the interaction of TLRs and NLRs gives rise to the multiprotein complex known as the inflammasome, which in turn activates secretion of mature interleukin 1 beta and interleukin 18. Experimental data show that innate immune receptors, the inflammasome components, and proinflammatory cytokines play crucial roles not only in sepsis, but also in organ-induced dysfunction, especially in the kidneys. In this review, we discuss the significance of the innate immune receptors in the development of acute renal injury secondary to sepsis. (AU)

Processo FAPESP: 07/07139-3 - Investigando o papel da heme-oxigenase 1 em diferentes processos inflamatórios renais em modelos animais
Beneficiário:Niels Olsen Saraiva Câmara
Linha de fomento: Auxílio à Pesquisa - Temático
Processo FAPESP: 08/55447-1 - Papel dos NOD-like receptor (NLR) na fisiopatogenia de insuficiência renal aguda (IRA) isquêmica e séptica
Beneficiário:Giselle Martins Gonçalves
Linha de fomento: Bolsas no Brasil - Pós-Doutorado